Brain, spinal cord, and peripheral nerves {nerve} have pathways.
Brain and spinal cord float in fluid {cerebrospinal fluid}|. Cerebrospinal fluid is in central canal and between neuron layers. Brain cells in central-canal enlargements make cerebrospinal fluid.
Neuron clusters {ganglia}| {ganglion} coordinate reflex arcs over body region to perform function. Ganglia have cell bodies in center and axons on outside. Ganglia perform orienting responses, focus attention, detect features, select behavior patterns, and initiate behavior sequences.
Nerves can have nerve-process outgrowths {neurite}.
Axons can contact both neuron and interneuron {synaptic triad}. Synaptic-triad processing can turn tonic signal into phasic signal.
Nerve ganglia can group {plexus}|.
Plexus {solar plexus}| {celiac plexus} behind stomach near celiac artery is largest autonomic center and controls adrenal gland secretion and intestine contraction.
Motor nerves {autonomic nervous system}| (ANS) connect to glands and non-striated smooth muscles and are always active. ANS controls heart, lungs, digestive tract, bladder, sweat glands, hair muscles, iris muscles, and arterioles. Such control relates ANS to emotion. Autonomic nervous system has sympathetic autonomic system and parasympathetic autonomic system.
Intestinal sensory nerves {enteric nervous system} measure distension and toxicity, making people feel full or nauseous [Gershon, 1998].
Brain and spinal cord nerves {central nervous system}| (CNS) connect to peripheral nerves in spine and body. Most CNS motor nerves go to voluntary muscles. Some CNS motor nerves go to glands and smooth muscles and are in autonomic nervous system.
Body nerves {somatic nervous system} {peripheral nervous system}| (PNS) can go to muscles, skin, and mucous membranes, or go to smooth muscles and glands, and are in autonomic nervous system. PNS includes 12 cranial-nerve pairs and 31 spinal-nerve pairs.
Central and peripheral nerves {parasympathetic autonomic system}| {parasympathetic nervous system} can stimulate micturition, defecation, alimentation, and sexual function.
Central and peripheral nerves {sympathetic autonomic system}| {sympathetic nervous system, function} can inhibit smooth-muscle cells.
functions
They regulate temperature by secreting sweat. They contribute to threat and aggression behaviors. They dilate pupils. They make hair stand on end. They control blood distribution throughout body by dilating or constricting blood vessels. They contribute to male sexual activities.
chemicals
Sympathetic-nervous-system postganglionic aminergic neurons synthesize and release noradrenaline. In sympathetic autonomic ganglia, presynaptic cholinergic fibers excite acetylcholine neurons and LHRH-like-peptide neurons. LHRH-like-peptide diffuses several micrometers to make slow excitatory postsynaptic potential (EPSP).
Human brains {brain} have divisions and cephali [Braak, 1976] [Braak, 1980] [Brodmann, 1914] [Bullock et al., 1977] [Caplan, 1980] [Carter, 1999] [Carter, 2003] [Crick and Jones, 1993] [Crick and Koch, 1998] [Ewert, 1980] [Glynn, 1999] [Harrison et al., 2002] [Heeger et al., 2000] [Hilgetag et al., 1996] [Jastrow, 1981] [Johnson, 1986] [Kessel and Kardon, 1979] [Kimura, 1992] [Le Bihan et al., 2001] [La Cerra and Bingham, 2002] [Logothetis, 2002] [Logothetis et al., 1999] [Logothetis et al., 2001] [Mathiesen et al., 1998] [Rees et al., 2000] [Rempel-Clower and Barbas, 2000] [Schüz and Miller, 2002] [Shepherd, 1991] [Waxman, 2000] [Webster et al., 1994] [Young, 2002] [Zeki, 1993].
neuron number
Human brains have 10 billion neurons.
weight
Human brain is 2% of body weight. Larger brains can dissipate heat better.
Two genes control brain size.
size compared to body size
Brain size, energy, and metabolism vary with body size to the 3/4 power, as determined by blood-vessel or neuron-axon branching patterns.
species
Elephant-nosed fish {mormyrid} live in muddy water. Mormyrids have relatively large brains, because they have electric organs and electroreceptors.
Rays and sharks are predators and have relatively large brains.
Warm-blooded animals have relatively large brains, to improve predation.
Fruit eaters and carnivores have relatively large brains compared to insect and leaf eaters. Fruit eating and meat eating require smaller digestive systems.
Primates have big brains. Bigger brains require more time to mature, fewer babies, and longer time between babies, so primates live longer than most species. Larger relative neocortex size associates with bigger social groups in primates.
individuality
Brains differ greatly in structure and connectivity.
Most animals have similar brain-volume to body-volume ratios {encephalization quotient} (EQ). Mammals have ratio seven times more than average. Chimpanzees have ratio three times more than average. Dolphins have higher EQ than great apes.
Brain has axon tracts {peduncle}.
Cell bodies and unmyelinated axons {gray matter}| are 60% of brain volume. Unmyelinated axons are 55%. Cell bodies are 5%.
Myelinated axons {white matter}| are 40% of brain volume.
Anterior cingulate gyrus, cortex, and basal ganglia make circuit {anterior attention network} that detects expected location. Cortex notes matches, and basal ganglia note mismatches.
Dorsolateral prefrontal cortex, cingulate nucleus, frontal eye fields in area 8, posterior parietal lobe in area 7a, pulvinar nucleus, and superior colliculus change object attention {attention shift} [Astafiev et al., 2003] [Corbetta, 1998] [Kustov and Robinson, 1996] [Mountcastle et al., 1981] [Sheliga et al., 1994] [Shepherd et al., 1986] [Wurtz et al., 1982].
The largest descending fiber tract {corticospinal motor tract} has one million axons from primary motor, supplementary motor, and premotor cerebral cortex layer-5 pyramidal neurons to spinal cord segment neurons to control precise finger and toe movements. Spinal-cord axons initiate skilled muscle movements at alpha motor neurons. Pre-central gyrus has the most corticospinal motor-tract neurons.
Lateral corticospinal tract, only in mammals, controls voluntary muscles. Anterior corticospinal tract does not cross over and is for posture and trunk position.
Signals from skin, muscles, tendons, and joints travel in spinal-cord dorsal column large and fast fibers to gracile nucleus and cuneate nucleus, then to thalamus medial lemniscus, then to post-central gyrus {dorsal-column-medial-lemniscal pathway} {DCML pathway}, which is for reflexes and rapid movement.
Axons from retina nasal halves, after traveling in optic nerve, cross over {decussation, axon} to other side in brain front middle optic chiasma.
Tracts {extrapyramidal tract} can include caudate nucleus, globus pallidus, putamen, red nucleus, reticular formation, and substantia nigra unmyelinated axons.
Between thalamic and cortical regions, one connection is feedforward {feedforward circuit}, and the other is feedback {feedback circuit}. Connections never combine both.
feedforward
Feedforward axons begin in layers 2 and 3 and end in layer 4.
feedback
Feedback axons begin in layers 5 and 6 and end in layers 1, 2, 3, and 6. Feedback goes to larger regions than feedforward [Barone et al., 2000] [Bullier, 2001] [Bourassa and Deschenes, 1995] [Cauller and Kulics, 1991] [DiLollo et al., 2000] [Grossberg, 1999] [Grossenbacher, 2001] [Heimer, 1971] [Hupe et al., 1998] [Johnson and Burkhalter, 1997] [Lamme and Roelfsema, 2000] [Lamme and Spekreijse, 2000] [Kosslyn, 1980] [Kosslyn, 1994] [Kosslyn, 2001] [Ojima, 1994] [Pollen, 1995] [Pollen, 1999] [Pollen, 2003] [Rhodes and Llinás, 2001] [Rockland et al., 1997] [Rockland, 1994] [Rockland, 1996] [Rockland, 1997] [Rockland and Van Hoesen, 1994] [Salin and Bullier, 1995] [Supèr et al., 2001] [Wiener, 1947] [Williams and Stuart, 2002] [Williams and Stuart, 2003].
Networks {frontal lobe attentional network} can be for attention, executive functions, decision making, voluntary movements, and stimulus conflict resolution [Mountcastle et al., 1981] [Wurtz et al., 1982].
Cerebrum, basal ganglia, brainstem, and cerebellum send to motor-neuron reciprocal-inhibition neurons {internuncial neuron}.
Systems {interoceptive system} can control homeostasis and chemical changes. Hypothalamus can sense molecules that can cross blood-brain barrier. Circumventricular organs, brainstem area postrema, and cerebrum subfornical organs lack blood-brain barrier and can sense large molecules.
Networks {limb premotor recurrent network} can spread positive feedback for limb command generation. Purkinje-cell bands converge on small nuclear-cell clusters in topographically organized recurrent circuits, with thalamic, motor cortical, rubral, pontine, and lateral-reticular neurons, which send commands to spinal cord along corticospinal and rubrospinal fibers.
A pain-sensing system {nociceptive system} {nociceptive pain response} can use superior colliculus, spinal cord, and thalamus neurons. It has opiate receptors, so opiates can inhibit it. Tactile, nociceptive, and thermal receptor systems interact.
Axons from each-retina nasal half, after traveling in optic nerve, cross over {decussation, optic nerve} to other side in brain front middle {optic chiasma}. Temporal-lobe half-retina axons, after traveling in optic nerve, remain on same side at optic chiasma, so visual-field right half goes to right lateral geniculate body and cerebrum, and left half goes to left.
Brain networks {premotor network} can control eye movements using recurrent pathways.
functions Separate premotor networks control smooth and saccadic eye movements. Separate premotor networks control horizontal and vertical movements.
input
Premotor network receives vestibular-sense input from semicircular canals. Vestibular nucleus signals use velocity coding. On brainstem sides, medial-vestibular-nucleus neurons interconnect with prepositus-hypoglossius neurons and with intermediate types. Prepositus hypoglossius neuron signals use position coding. Brainstem sides interconnect through recurrent inhibitory pathway.
Mammalian tracts {pyramidal tract} can excite motor neurons and enhance reflexes. Muscle actions, but not skilled-movement learning or memory, require pyramidal tract, which is bigger if cortex is bigger.
Septum and hippocampus circuit {septo-hippocampal system} affects contextual and spatial memory.
Perirhinal cortex receives multisensory input and sends to hippocampus, which sends to diencephalon {short-term memory circuit} to make short-term memory [Aksay et al., 2001] [Compte et al., 2000] [Courtney et al., 1998] [de Fockert et al., 2001] [Eichenbaum, 2002] [Fuster, 1973] [Fuster, 1995] [Fuster, 1997] [Gazzaniga, 2000] [Goldman-Rakic, 1992] [Goldman-Rakic, 1995] [Goldman-Rakic et al., 2000] [Miller, 1999] [Miller et al., 1996] [Pochon et al., 2001] [Rao et al., 1997] [Romo et al., 1999] [Squire and Kandel, 1999] [Squire, 1992].
Vibration, steady pressure, and light touch information goes from skin, to spinal-cord dorsal root, to brainstem lower end, to thalamus ventro-basal complex, and to primary somatosensory cerebral cortex {skin sensory circuit}. All senses have similar circuits.
Body systems {somatosensory system} can have viscera, vestibular, proprioception, and kinesthesia systems and autonomic, homeostasis, and fine touch functions. Somatosensory system uses reticulum, monoamine nuclei, acetylcholine nuclei, hypothalamus, basal forebrain, insular cortex, S2 cortex, and medial parietal cortex.
Body systems {spatial attention system} can regulate inferotemporal neurons and filter inferotemporal-area input from selected stimulus and memory, for pattern recognition.
Proprioception input goes to nucleus dorsalis, then to ipsilateral dorsal spinocerebellar tract or to contralateral ventral spinocerebellar tract, then to cerebellum, and then to cerebral cortex {spinocerebellar tract}. Dorsal and ventral spinocerebellar tracts are for movement initiation or for position information from muscle spindles, Golgi tendon organs, and touch receptors.
Tracts {spinoreticular tract} can be for dull and chronic pain from soma.
Diffuse touch, pressure, acute pain, and thermal fibers {spinothalamic pathway} {spinothalamic tract} {protopathic pathway} {spinothalamic system} go to substantia gelatinosa as unmyelinated fibers, cross to contralateral spinothalamic tracts, go through reticular system, go to thalamus ventral posterior nucleus, and end at cerebrum. Spinothalamic tract has small and slow feedback nerves for pain inhibition.
Older unconscious visual pathway {tectopulvinar pathway} {tectofugal pathway} goes from tectum to superior colliculus, thalamus pulvinar nucleus, and parietal lobe and is for visual spatial orientation, orienting responses, and movement to focus attention. Geniculostriate and tectopulvinar pathways interact [Ramachandran, 2004].
Spinal-cord tracts {tectospinal tract} can be for reflex head turns.
Pathways {vestibulo-ocular pathway} from retina to vestibular system to cerebellum can allow eye to track moving objects smoothly while head turns.
Spinal-cord tracts {vestibulospinal tract} can be for posture reflexes.
Circuits {dorsal system} {dorsal pathway} {vision-for-action} {where pathway} {how pathway} {high path for vision} {ambient system} can go from occipital lobe area V1 to mediotemporal (MT) area, parietal area PG, posterior parietal area (PPC), and dorsolateral prefrontal cortex [Bridgeman et al., 1979] [Rossetti, 1998] [Ungerleider and Mishkin, 1982] [Yabuta et al., 2001] [Yamagishi et al., 2001].
functions
Dorsal pathway processes object location, size, parts, and characteristics. It converts spatial properties from retinotopic coordinates to spatiotopic coordinates. It tracks unconscious motor activity and guides conscious actions, such as reaching and moving eyes.
output
Dorsal system sends to amygdala and hippocampus to form visual memories [Heimer, 1971].
Circuits {ventral system} {vision-for-perception} {what pathway} {low path for vision} {focal system} can go from occipital-lobe area V1, through areas V2 and V3 and V4, to inferior temporal lobe area TE, limbic system, and ventrolateral prefrontal lobe [Bridgeman et al., 1979] [Epstein and Kanwisher, 1998] [Haxby et al., 2001] [Heimer, 1971] [Ishai et al., 2000] [Milner and Goodale, 1995] [Ungerleider and Mishkin, 1982].
functions
Ventral system is for recognition. It classifies stimuli shapes and qualities. It registers new category instances. It responds to patterns, shapes, colors, and textures, with earlier neurons for smaller and later neurons for bigger. It does not contain representations but organizes input into familiar packets.
output
Ventral system sends to amygdala and hippocampus to form visual memories.
Cerebrum spatiotemporal firing patterns {brain code} {cerebral code} can represent actions or perceptions.
switches
Neurons are switches. They contrast below-threshold with above-threshold.
coding
Contrast or mark sequences can be codes and carry messages. Each millisecond, axon locations either have or do not have spikes.
Times between spikes can code for timing intervals.
Number of spikes per second reflects average voltage difference at axon hillock.
coding: types
Perhaps, neuron code uses average number of spikes per 100 millisecond {firing rate code}. Perhaps, neuron code uses spike timing {temporal coding}, for synchronization and oscillation.
Perhaps, neuron code is probabilistic [Rao et al., 2002].
Perhaps, neuron code uses synchronous firings {synfire chain model} [Abeles, 1991] [Abeles et al., 1993].
Perhaps, neuron code uses precisely timed spike or burst {first-time-to-spike model} [VanRullen and Thorpe, 2001].
Perhaps, brain uses standing, traveling, rotating, or compression waves [Ermentrout and Kleinfeld, 2001].
contrast
Contrast is relative intensity, intensity difference or ratio.
contrast: space
ON-center neurons have excitation when input is on their receptive-field center and inhibition when input is on annular region, so they detect contrast between central and annular regions. OFF-center neurons have excitation when input is on annular region and inhibition when input is on center.
ON-center neurons pair with OFF-center neurons and work together to enhance contrast.
contrast: opposites
Opponent-process neurons detect receptor-input ratio and so contrast extremes.
contrast: categories
Categorization neurons use thresholds to establish and contrast categories.
contrast: orientation
Cortical neurons in orientation column pair with neurons in orientation column for perpendicular or other orientation. They also pair with neurons for no orientation. The pairs enhance contrast.
contrast: process
Neurons and neuron pairs find relative values and so contrast by lateral inhibition, spreading activation, and comparing opposite receptors.
contrast: boundaries
Contrast between two things marks a boundary or threshold. No value difference means both are the same, with no boundary, mark, point, or information. Markers/boundaries are information bits. Contrasts, markers, or boundaries are like ON or OFF, 0 or 1, YES or NO. Markers provide signs or landmarks, such as indexes, for references, to which other signs can relate.
contrast: boundaries and space
Boundaries are markers in space. The idea of space depends on the idea of boundary. Boundaries separate two regions, such as self and not-self or inside and outside.
Codes {bursting} can use spike bursts followed by quiet periods [Crick, 1984] [Koch, 1999] [Koch and Crick, 1994] [Lisman, 1997].
Perhaps, neuron code uses neurons with precise ranges {population coding} {pattern coding} {Across-Fiber Pattern theory}. For example, movement trajectories can be sums of many neuron outputs. Brains can store representations as values in neuron sets. Repeated input activates same neuron population. Similar input activates similar neuron population. Difference between two patterns is quantitative difference between populations. With population coding, patterns and concepts have geometry [Hahnloser et al., 2002] [Perez-Orive et al., 2002].
Perhaps, for each stimulus, brain has one receptor and one neural path {labeled line}.
Perhaps, neuron code uses few neurons with precise location or distance {sparse coding} [Hahnloser et al., 2002] [Perez-Orive et al., 2002].
Perhaps, neuron code uses few spikes with precise timing {sparse temporal coding} [Hahnloser et al., 2002] [Perez-Orive et al., 2002].
Brain performs computations {brain computation}. Brain scanning and brain lesion analysis shows that brain regions mediate brain functions {localism}. Brain regions have functions, and brain functions involve several brain regions coordinating sequentially and simultaneously [Carter, 1999].
input and output
Neuron populations receive input-signal sets and calculate output-signal sets. For functions, brain has several paths that make same output from same input.
All central-nervous-system input goes to cerebellum, reticular formation, and thalamus. Input that can eventually cause sense qualities goes to sense neurons in thalamus and then cerebrum. Brain inputs and outputs coordinate. For example, motor neurons and muscle receptors link.
input and output: global information
All brain information uses many neurons, which process only local information, but result is global [Black, 1991].
input and output: convergence
Inputs from different cortical regions {convergence region, vision} converge on cortical regions {convergence zone}. Convergence-zone output includes feedback to input cortical regions. Brain has more than 1000 convergence regions and more than 100 convergence zones.
input and output: distributed processing
Brain has many recurrent, lateral intracortical connections, and neurons receive from large spatial area. No neuron has simple direct circuit [Abbott et al., 1996] [Dayan and Abbott, 2001] [Rao et al., 2002] [Rolls and Deco, 2002] [Shadlen et al., 1996] [Zhang et al., 1998].
More than 50% of cortical neurons send output to distant cortical areas.
input and output: important information
Brain gives command to region with the most-important information.
coding
Information theory applies to neural coding, and one impulse can carry more than one information bit [Rieke et al., 1996] [Shannon and Weaver, 1949].
coding: repetition
Brain cells typically experience same correlations, associations, and comparisons many times. Processing in small brain region repeats often. Repetition improves efficiency as cells modify.
coding: electrochemical coding
Axon ion flows change voltage, and receptor-membrane neurotransmitters change voltage, so neuron coding is electrochemical.
coding: discrete coding
Neurons generate neurotransmitter packets and action potentials, rather than graded potentials, so information flows are discrete on-or-off sequences rather than continuously-varying voltages or currents.
coding: frequency code
Neuron impulse frequency indicates both time interval and intensity. Spike frequency F above normal frequency NF is constant C times power p of receptor displacement X from normal N: (F - NF) = C * (X - N)^p.
Neuron spike frequency never exceeds 800 spikes per second and never becomes 0. At rest, frequencies can be few per second or hundreds per second.
coding: information amount
If axon-hillock depolarization or no depolarization can happen every millisecond, millisecond intervals are either on or off. In 100 milliseconds, 2^100 bits can travel down axon. 2^100 bits is approximately 10^30 bits, which is approximately 1000^10 bits.
If number of possible letters, digits, and punctuation marks is 1000, 1000^10 bits can represent ten-letter words, labels, indexes, or pointers, so one neuron acting for 100 milliseconds can code for any ten-letter word. One hundred thousand neurons acting for 100 milliseconds can code for any million-letter string. One hundred thousand neurons acting for 100 milliseconds can code for any million-dot image, if dots can have 1000 levels of gray and color.
One hundred neurons acting for one millisecond can code for any ten-letter word. One neuron acting for 10^7 milliseconds, approximately 3 hours, can code for any million-letter string or million-dot image.
coding: summation
Axons depolarize for percentage of time. In time intervals, such as ten milliseconds, so short that receptors do not have time to change, depolarization sequences with same total number of depolarizations have equivalent physiological effects, no matter in what order signals arrived. In these cases, axon coding is not a significant factor, and irregular conduction rates do not matter. Ten-millisecond intervals have 10 instants that can be ON or OFF, and so intervals have 2^10 different possible sequences. However, such short time intervals have only 11 physiological possibilities: 0 to 10 total depolarizations.
computations
Neurons promote, amplify, block, inhibit, or attenuate signals. Neuron circuits can lower thresholds, switch signals, amplify signals, filter frequencies, set thresholds, control currents, direct flows, induce currents, control voltages, compare signals in time and space, add quantities, multiply quantities, and perform logical operations.
Most visual cortical neurons respond to line contrasting with background. Output maximizes if contrast is in receptive-field middle. Response falls off rapidly as contrast line moves to either side. Function looks like Gaussian distribution with large variance or looks like two sigmoidal functions joined at maximum. Most neurons behave like Gaussian HBF units, rather than multilayer-perceptron (MLP) sigmoidal units.
computations: potentiation
Nitric oxide from receptor neuron maintains sending-neuron long-term potentiation (LTP). Cyclic AMP second messenger sensitizes receptor neuron. NMDA glutamate receptors sensitize receptor neuron. Potentiation makes neuron reach threshold with lower input than normal excitation level.
computations: association by neurons
Interneuron can detect stimulus timing and amplitude between two pathways. Two pathways can both contact an interneuron that controls secondary circuit. If both pathways carry current simultaneously, secondary circuit maintains current. If both pathways carry no current or only one has current, secondary circuit has no current. Interneuron detects simultaneous pathway activation.
computations: conditional statement
Depolarization can happen only if all inputs to neuron are active. Depolarization can happen if one input to neuron is active. Depolarization can happen only if some inputs are active and some inactive.
computations: difference
Neurons compare signals to detect change or difference, rather than absolute values.
computations: feedback
Neuron circuits with excitatory and inhibitory feedback have short, synchronous discharges in local clusters.
computations: indexing system
Brains have index list to rapidly locate information.
computations: inhibition
Inhibition dampens neuron signals and more quickly returns neurons to resting states, allowing shorter time intervals and quicker responses. Between two stimuli, inhibition increases stronger signal and decreases competing weaker stimulus. Thus, inhibition can enhance weak stimulus that has only weaker stimuli nearby in space or time.
computations: inverse model
If supplied with sample responses, inverse model can predict input commands.
computations: movement initiation
Movement initiation and programming are separate asynchronous processes. Deciding to perform action corresponds to building positive feedback in limb premotor network.
computations: movement programming
Movement initiation and programming are separate asynchronous processes. Cerebellar cortex programs which movement to perform. Programming can happen while preparing movement or moving.
computations: positive whole numbers
Synaptic transmission uses neurotransmitter-molecule packets. Axon depolarizations are independent and countable. Therefore, neurons use whole number calculations and whole number ratios, with no fractions or real numbers. Because neurotransmitter molecules and axon depolarizations have no opposite, neurons use only positive numbers, never negative numbers.
computations: synchronizing
Neuron reciprocal interactions can synchronize signal phase, if reciprocal signal delay is less than one-quarter oscillation. Neuron excitatory reciprocal connections can find feature relations by enhancing, prolonging, and synchronizing neuron responses.
computations: timing
Brain uses time-delay circuits, inhibitory signals, and circuit-path rearrangements to time neuron events.
computations: transformations
Brain can use geometric ratios, translations, rotations, and orientations to represent distances and manipulate lines and shapes.
validation
Brain sends inputs along several paths to cross-validate processing and representations by comparing redundant process outputs.
Interneurons can associate reflex-pathway nerve-cell states with other reflex-pathway nerve cell states {association triad neuron mechanism}.
interneurons
Nerve cells in pathways from sensation to action connect using interneurons for cellular associative learning. Interneurons laterally excite or inhibit main neurons.
process
Cell that is to learn inhibits interneuron. Interneuron excites learning cell and inhibits paired cell. Paired cell inhibits interneuron and learning cell.
Associative learning requires asymmetric connections. Both main neurons inhibit interneuron, but interneuron excites learning neuron and inhibits paired neuron. Paired cell inhibits learning cell, but learning cell does not synapse on paired cell.
process: input
Association requires simultaneous stimuli to both sense cells.
process: circuit
After stimuli cease, asymmetric association-triad circuit causes signals to continue to flow around neurons, keeping learning-cell electric potential smaller. This makes it easier to stimulate learning cell.
When paired stimuli end, paired cell stops inhibiting interneuron and learning cell, so interneuron excites learning cell more. Learning cell has decreased inhibition and so inhibits paired cell even more, keeping state going until unpaired stimuli disrupt positive feedback, so neurons return to normal.
simplicity
Association nerve triad is simplest associative learning system. One neuron alone can only sensitize or desensitize itself. Two neurons can only have reverberation. No other three-neuron arrangement can make a learning circuit.
Interneuron must have inhibition by path neurons, so interneuron voltage increases when stimulation stops. Interneuron must stimulate learning cell, so learning-cell voltage increases after stimulation stops. Paired cell must inhibit learning cell, so learning-cell voltage increases after stimulation stops. Interneuron must inhibit paired cell, so, as interneuron increases voltage, paired-cell inhibition decreases.
There must be no connection from learning cell to paired cell. If there is inhibition, stimulation end increases paired-cell inhibition on learning cell. If there is excitation, stimulation end decreases inhibition, but excitation mimics stimulation, so there can be no excitation between direct paths.
There is no interneuron excitation, because stimulation end only quiets them.
uses
Association does not detect current or no current in one or the other pathway, only simultaneous inputs.
uses: negative association
If sense cell inhibits learning cell, circuit still works by positive feedback but in reverse, so voltage difference becomes more. This makes learning cell more difficult to stimulate.
uses: attention
Association allows attention-like input acknowledgement.
uses: reflex control
Reflexes receive signals from sensors and activate muscles. Association triads can control reflexes by signals from other nerve pathways or from brain.
uses: time
Association triads can detect simultaneity in time.
uses: space
Association triads can detect simultaneity in space. Time can code spatial distance.
uses: intensity
Association triads can compare intensities. Time can code intensity.
Nerve pathway {labeled-line code} itself indicates stimulus nature and spatial location.
Cortex mechanisms enhance and suppress synapses and redistribute axon terminals among receptors {neuromodulatory system}. First, synapses receive non-specific input from cholinergic and noradrenergic neurons. Later, they receive input from both body sides [Crick and Koch, 1998].
Command passes to region with the most-important information {principle of redundancy of potential command} {potential command redundancy} {redundancy of potential command}.
Cortical-neuron axons from sense brain areas can re-enter brain areas {re-entry} {re-entrant pathway}. Re-entry synchronizes and coordinates but does not provide feedback. Most nerve pathways send signals back to starting points after one or more synapses. Memory depends on brain pathways that re-excite themselves.
Control system models {Smith predictor} can predict responses if supplied with sample commands. Smith predictors combine delayed and undelayed control system models to build controller for systems with large time delays.
Nearby neurons inhibit neuron {lateral inhibition}|, to increase contrast.
Excitation tends to spread through region {spreading activation} {spreading excitation}, to link regions.
People can measure scalp electric-voltage waves {electroencephalography}| (EEG).
cause
EEG wave voltages are sums of graded potentials in dendritic trees and their synapses [Creutzfeldt and Houchin, 1984] [Creutzfeldt, 1995] [Freeman, 1975] [Mountcastle, 1957] [Mountcastle, 1998] [Remond, 1984].
EEG potential changes are larger than neuron induced activity. Potential differences between cell bodies and neuron fibers influence EEG waves. Brain potential waves imply synchronized neuron activities, over distances more than two millimeters apart. Waves are coherent, not harmonic, across different cortical areas.
location
Electric waves appear in parietal lobe, then primary motor cortex and occipital lobe, and then prefrontal lobe.
amplitude
EEG wave voltages are 1 mV to 2 mV. To detect voltage change requires averaging hundreds of measurements to subtract noise. EEG can measure scalp potential differences less than 100 microvolts [Makeig et al., 2002].
correlations
Scalp evoked-potential changes in response to image, sound, or mental event [Galambos et al., 1981].
Anesthesia and responses to simple stimulus configurations can have prolonged brain potential synchronization. Brain-potential synchronization is less during awake states and complex situations.
Waves are large in tasks requiring activity integration across different cortical areas. Waves stop at perceptual-processing conclusion and motor-signaling beginning.
Waves do not carry information about stimuli nor relate to signals from individual neurons.
correlations: awake
Hippocampus has theta rhythm at 4 Hz to 10 Hz during active movement and alert immobility, synchronized between hemispheres and 8 mm along hippocampus longitudinal axis. Awake brain has synchrony, which increases with attention and preparation for motor acts. Brain potential synchronization is less when awake.
Other behaviors have local and bilaterally synchronous rhythm near 40 Hz.
200-Hz waves correlate with alert immobility.
A 12-millisecond phase shift goes from brain rostral to caudal pole, during alpha wave activity while awake.
Most waves during waking are in posterior cortex, lower than vertex.
correlations: sleep
EEG waves can differentiate seven sleep stages. Most waves during sleeping are in vertex and frontal lobe. Synchronous firing characterizes deep sleep and epilepsy.
Between waking and sleeping, brain wave change is abrupt in adults. Between waking and sleeping, brain wave change is slow in children.
correlations: slow-wave sleep
NREM sleep has low-frequency, high-amplitude waves. Non-REM-sleep phases 3 and 4 have low-frequency EEG waves {slow-wave sleep}.
correlations: REM sleep
Awake and REM sleep activation level has high-frequency, low-amplitude waves [Hobson, 1989] [Hobson, 1994] [Hobson, 1999] [Hobson, 1999] [Hobson, 2002] [Hobson et al., 1998].
correlations: other waves
EEG waves include bereitschaftspotential, contingent negative variation (CNV), and motor potential.
factors: age
EEG-wave localization, regularity, continuity, similarity from both hemispheres, synchrony from similar areas, and stability increase until age 35. Brain-wave amplitude decreases until age 35.
Alpha waves disappear when eyes open or people have mental imagery {alpha blocking}, but some visual activities do not block alpha waves. If both visual hemispheres have damage, alpha rhythm stops.
EEG waves {alpha wave} can have frequency range 8 to 12 per second. Sleep or quiet rest has alpha waves. They have larger amplitude if brain has pathology. A 12-millisecond phase shift goes from brain rostral to caudal pole, during alpha wave activity while awake and during REM sleep [Varela et al., 2001]. Alpha-wave frequency increases until five or six years old.
Electric potentials {auditory evoked potential} (AEP) happen after sounds [Creutzfeldt and Houchin, 1984] [Creutzfeldt, 1995] [Freeman, 1975] [Mountcastle, 1957] [Mountcastle, 1998] [Remond, 1984]. Scalp electrodes can record them.
sleep
AEP during waking and REM sleep are similar but differ from AEP during non-REM sleep. Early AEP do not fluctuate during sleep-waking cycle. Early thalamocortical activity causes middle AEP, which decrease amplitude from waking to stage-4 sleep but are normal in REM sleep.
Later, AEP amplitudes decrease from waking to stage-4 sleep but increase in REM sleep. P20 component reflects cerebral-cortex activity and increases from waking to stage-4 sleep but returns to waking level in REM sleep. REM sleep does not have latest AEP: P100 wave, P200 wave, and P300 wave.
EEG waves {beta wave} can have frequency range 15 Hz to 25 Hz. Beta-wave frequency increases until 15 years old.
EEG {bispectral index} can measure anesthesia depth.
EEG waves {delta wave} can have frequency range 1 Hz to 4 Hz. If sound is during REM-sleep delta-wave activity, no coherent 40-Hz oscillations begin [Creutzfeldt and Houchin, 1984] [Creutzfeldt, 1995] [Freeman, 1975] [Mountcastle, 1957] [Mountcastle, 1998] [Remond, 1984]. Delta-wave frequency increases until one year old.
Scalp potential {evoked potential} {event-related potential} changes in response to image, sound, or mental event [Galambos et al., 1981].
Concentrating on probable signal arrival changes electroencephalograph potential {expectancy wave} (e-wave).
Awake but non-attentive animals have large-amplitude synchronized 25-Hz to 35-Hz oscillations {gamma wave} [Engel and Singer, 2001] [Keil et al., 1999] [Klemm et al., 2000] [Revonsuo et al., 1997] [Rodriguez et al., 1999] [Tallon-Baudry and Bertrand, 1999].
locations
Visual precentral and postcentral cortex, retina, olfactory bulb, thalamus, other brain nuclei, and cerebral neocortex have continuous and coherent 30-Hz to 70-Hz {40-Hz oscillation} electric potential oscillations.
All visual areas and both hemispheres synchronize cells. Visual field feature produces coherent 40-Hz oscillations separated by as much as 7 mm in visual cortex [Eckhorn et al., 1988] [Eckhorn et al., 1993] [Engel et al., 1990] [Friedman-Hill et al., 2000] [Gray and Singer, 1989] [Kreiter and Singer, 1992] [Ritz and Sejnowski, 1997].
Somatosensory and motor cortex potentials synchronize while thinking but vanish during actual movement.
cause
40-Hz oscillations happen when cells in different cortex or thalamus parts respond to linked stimulus parts [Crick and Koch, 1990] [Engel and Singer, 2001] [Metzinger, 2000].
attention
Oscillations synchronize more during focused attention [Mountcastle et al., 1981] [Wurtz et al., 1982].
induced gamma wave
When people perceive object with coherent features, 30-Hz EEG wave starts in occipital cortex 200 ms after stimulus and dies out after perceptual processing.
People can measure magnetic fields caused by brain electric currents {magnetoencephalography} (MEG), using superconducting quantum interference devices (SQUID).
When people make or observe voluntary movement, EEG waves {mu wave} {µ wave} decrease. Mirror neuron activity blocks mu waves.
EEG waves {N400 wave} can be about semantic improbability, as opposed to semantic relatedness.
260 ms to 500 ms after rare stimuli, attention to object to recognize it or use it causes 40-Hz oscillations {P300 wave}, which correlate with event unexpectedness.
If people are conscious or dreaming, high-amplitude electrical waves {PGO wave} arise in pons, radiate to geniculate body, and then go to occipital cortex. Saccadic eye movements cause potential waves in cholinergic neurons in pons and go to lateral geniculate nucleus and occipital cortex. Signals from aminergic cells inhibit cholinergic neurons. PGO waves accompany desynchronization.
0.8 second earlier than planned voluntary movement, ipsilateral motor cortex EEG changes potential {readiness potential} to negative. Conscious willing feeling is later. 0.5 second earlier than unplanned voluntary movement, EEG changes potential to negative. Perhaps, consciousness can still stop or allow action before it has begins [Libet, 1993] [Libet et al., 1999]. Lateralized readiness potential is in contralateral cortex and happens after action selection.
For activation, awake stage and REM sleep has high-frequency low-amplitude EEG waves. NREM sleep has low-frequency high-amplitude EEG waves. Stage II NREM sleep has distinctive EEGs {sleep spindle} {K-complex wave}.
EEG waves {theta wave} in hippocampus can have frequency range 4 Hz to 8 Hz [Buzsáki, 2002] [Kahana et al., 1999] [Klimesch, 1999] [O'Keefe and Recce, 1993]. Theta-wave frequency increases until two to five years old. REM sleep has theta waves in hippocampus.
Treatments {Transcranial Magnetic Stimulation} (TMS) can excite or inhibit brain regions to treat depression, obsession, stress, and mania [Cowey and Walsh, 2001] [Kamitani and Shimojo, 1999].
Brain evolved {brain, evolution}.
brain: parts
Brain is an enlargement and opening of spinal cord cranial end. First, slight enlargement formed rhombencephalon. Then, pons (bridge) evolved. Rhombencephalon evolved to myelencephalon and metencephalon. Above pons and further forward, rostrally towards nose, is mesencephalon. From midbrain roof, special motor cerebellum evolved, first becoming large and important in birds. Fourth-ventricle top became midbrain cerebral aqueduct. Rostral to midbrain is forebrain, with diencephalon and telencephalon [Cummins and Allen, 1998].
brain: processes
Neural structures evolved first reflexes, then associations, then feature surfaces and flows, then objects and events, then scenes and trajectories, and then histories and stories over space and time using language [Cummins and Allen, 1998].
brain: tissue
Neural tissue evolved from neuron to interneuron, ganglion, ganglia group, cortex, two-layer paleocortex, four-layer neocortex, and six-layer frontal lobe cortex.
design
Neural tissue and brains evolved opportunistically and did not follow design. Brains are not evolving teleologically to defined final state. Brains do not necessarily work efficiently.
motion
Originally, sensation led directly to motion. Brain evolved to separate perception from motion. Brain further evolved to integrate perception, memory, emotion, and goals. Brain then evolved to have consciousness.
Mammalian cortex has both caudal and rostral reciprocal pathways {dual origin hypothesis}. Birds have hyperstriatum and neostriatum. Hyperstriatum evolved like mammalian cortex. Neostriatum evolved from DVR.
pallium
Top and bottom cerebral neocortex layers are homologous to pallium. Reptile medial pallium evolves to mammal hippocampus major and subiculum. Reptile lateral pallium evolves to mammal olfactory cortex. Pallium receives from olfactory and limbic cortex, caudally.
ventricular ridge
Middle four cerebral neocortex layers are homologous to reptile dorsal ventricular ridge. Dorsal ventricular ridge receives from within itself, rostrally.
Reptiles have dorsal cortical plate {pallium}.
Reptiles have a two-layer ridge {ventricular ridge} {dorsal ventricular ridge} (DVR) behind brain ventricles.
Enlargement and opening of spinal-cord cranial end at hindbrain was earliest brain {rhombencephalon}|.
Rhombencephalon evolved to medulla oblongata {myelencephalon}|, in hindbrain.
Above pons and further forward, rostrally towards nose, is midbrain {mesencephalon}|.
Rhombencephalon evolved to medulla, cerebellum, pons, mamillary bodies, pituitary gland, and habenula {metencephalon}|, in hindbrain.
Brain regions {rhinencephalon}| {smell brain, rhinencephalon} can be near frontal lobe.
Rostral to midbrain are epithalamus, fornix, hypophysis, hypothalamus, subthalamus, thalamus, and third ventricle {diencephalon}|, in cerebrum and forebrain. All diencephalon regions connect to each other and to cerebral cortex.
Rostral to midbrain are cerebral cortex, white matter, and basal ganglia {telencephalon}|. Cerebral cortex has frontal, parietal, temporal, occipital, insular, and limbic lobes.
evolution
In amphibians, dorsal telencephalon became dorsal cortex and hippocampus. Medial telencephalon became septum, which connects to hippocampus. Lateral telencephalon did nothing, because amphibians have no dorsal ventricular ridge. Ventral telencephalon became striatum, for muscle control.
In reptiles, dorsal telencephalon became dorsal cortex and hippocampus. Medial telencephalon became septum. Lateral telencephalon became dorsal ventricular ridge, for senses and/or emotions. Ventral telencephalon became striatum.
In birds, dorsal telencephalon became hyperstriatum with wulst. Medial telencephalon became septum. Lateral telencephalon became dorsal ventricular ridge. Ventral telencephalon became striatum.
In mammals, dorsal telencephalon became cerebrum, including neocortex and hippocampus. Medial telencephalon became septum. Lateral telencephalon became laterobasal amygdala for emotions. Ventral telencephalon became striatum.
Bottom brain has eight repeated parts {rhombomere}, with one next to cerebellum and eight near spinal cord. Cells do not migrate from one rhombomere to another. Eighth cranial nerve comes from fourth rhombomere.
Low brain part {lower brain} includes medulla oblongata, pons, and cerebellum.
Above spinal cord, bottom brain {hindbrain}| is medulla oblongata then pons.
Above pons and further forward, rostrally towards nose, are cerebellar peduncles, inferior olive, quadrigeminal plate, nucleus accumbens, red nucleus, substantia nigra, tectum, and midbrain tegmentum {midbrain}|. All midbrain nuclei have ascending and descending axon tracts. Midbrain is for attention, controls aggressiveness, and predicts adjustments to visual perception that will result from movement, using signal {central kinetic factor} that codes displacement direction and speed.
Rostral to midbrain are cerebral-cortex frontal, parietal, temporal, occipital, insular, and limbic lobes, white matter, and basal ganglia {endbrain}.
Front brain {forebrain}| contains cerebrum diencephalon and telencephalon: amygdala, basal ganglia, cortex, hippocampus, olfactory bulb, and thalamus.
At fourth ventricle, above spinal cord, brain regions {brainstem}| can have cervical flexure and cephalic flexure and contain midbrain and hindbrain [Parvizi and Damasio, 2001] [Zeman, 2001]. Brainstem includes cranial nerve nuclei.
hindbrain
Hindbrain contains pons near midbrain and medulla oblongata near spinal cord.
midbrain
Midbrain has noradrenergic lateral reticular system, noradrenergic locus coeruleus, serotoninergic raphe nucleus, dopaminergic basal midbrain nuclei, cholinergic sense nuclei, and histaminergic nuclei.
Histaminergic nuclei project in net over brain.
Cholinergic sense nuclei connect to cerebral cortex. Damage reduces cerebral activity and causes a dreamy state.
functions
Brainstem integrates signals for attention, sex, and consciousness. Consciousness requires higher brainstem.
Regions {area postrema} can lack blood-brain barrier and can sense large molecules.
Forward brainstem {basal forebrain}| damage affects event-time recall.
Brainstem nucleus {cochlear nucleus} receives from cochlea hair cells.
Brainstem nucleus {lateral cervical nucleus} sends to superior colliculi.
Brainstem nucleus {nucleus sagulum} sends to superior colliculi.
Brainstem nucleus {perihypoglossal nucleus} sends motor input to superior colliculi.
In vertebrates other than mammals, structure {poker chip} decides which of twenty behavior modes is most appropriate. Poker chip later evolves to become reticular formation.
Brainstem nucleus {posterior commissure nucleus} sends motor input to superior colliculi.
Brainstem nucleus {prepositus hypoglossius} receives from superior colliculi and sends to oculomotor system.
Mesencephalic reticular formation, intralaminar nuclei, and reticular nuclei {reticular formation}| {reticular activating system} {reticulum} {ascending reticular activating system} {extralemniscal system} {non-specific afferent system} {gating system} {ascending activation system} {midbrain reticular formation} {mesencephalic reticular formation} stimulate thalamus and cortex to cause waking and sleep states.
purposes
Reticular formation arouses, integrates signals, maintains consciousness, controls vital functions, modulates perception, forms and recalls memories, and coordinates motor behaviors.
purposes: consciousness
Consciousness involves thalamus reticular-activating-system ascending fibers.
damage
Damage to reticular formation causes coma, memory disorganization, sleep, reduced cortex energy, similar reactions to strong and weak stimuli, and poor behavior control.
electrical stimulation
Reticular-formation electrode stimulation can cause unpleasant feelings.
electrical stimulation: memory
Retention improves with reticular formation stimulation, which arouses brain. Stimulation does not affect retrieval. Stimulating other brain areas has no affect on retention.
biology: input
Reticular formation receives axons from sense pathways and cortex and has multisensory convergence sites. All senses activate ascending reticular formation, which mediates pain. Stimulating ascending reticular formation causes fear and avoidance behaviors.
biology: output
Interconnecting neurons with short axons run from lower brainstem to midbrain. Descending reticular formation acts on interneurons indirectly.
biology: chemicals
Serotonin affects reticular formation and attention system to synchronize cortex. Noradrenaline desynchronizes cortex.
biology: columns
Reticular formation has medial, median, and lateral columns, from anterior midbrain through pons, medulla, and spinal cord [Hobson, 1989] [Hunter and Jasper, 1949] [Magoun, 1952] [Moruzzi and Magoun, 1949] [Steriade and McCarley, 1990].
Medial column receives pyramidal tract, cerebellum, and sense axons from cortex and sends by ascending reticular activating system to intralaminar thalamic nuclei, which send to striatum and cortex, to activate cortex and control waking and sleeping.
Raphe nucleus median column, mainly dorsal raphe nucleus, sends inhibition to limbic system in median column.
Lateral reticular system for attention projects to spinal cord, hypothalamus, and brainstem lateral-column tractus-solitarius nucleus. Noradrenaline locus coeruleus lateral column sends attention information to limbic system and prefrontal lobes.
biology: evolution
Reticular formation is only in mammals but evolved from something similar in lower animals.
Brainstem nucleus {solitary tract nucleus} {tractus solitarius nucleus} receives from locus coeruleus, trigeminal nucleus, and vagus nerve and sends to parabrachial nucleus, which receives from GI tract, and ventral medial basal thalamus. Solitary tract nucleus, with taste cortex and thalamus, is for taste preferences and can detect nausea. NTS is satiation region and receives gut peptide cholecystokinin (CCK).
Brainstem nucleus {trigeminal nucleus} receives sensory C fibers and A-delta fibers caudally from spinal cord posterior horn lamina I and sends to ventral medial posterior thalamus, brainstem nucleus tractus solitarius, and brainstem parabrachial nucleus.
Brainstem nuclei {vestibular nucleus} can be for balance.
Brainstem regions {zona incerta} can send motor input to superior colliculi.
Ascending reticular-activating-system (ARAS) lowest-hindbrain component {sensory reticular formation} receives visceral, somatic, auditory, and visual axons from ascending sense axons and sends to neocortex through hypothalamus and thalamus. It has pain center and wakefulness or alertness center.
Spinal-cord brainstem bulb {medulla, brain}| {medulla oblongata} includes basal ganglia and continues major nerve tracts. It relays auditory nerve sense and motor nerves, mediating phonation and articulation. It regulates cardiac action, chewing, tasting, swallowing, coughing, sneezing, salivation, vomiting, and sucking in newborns. Respiratory center maintains respiration. Some medulla-oblongata neurons make epinephrine.
A limbic-system part {amygdala}| includes insula white matter.
location
Insula is in posterior frontal lobe and anterior temporal lobe.
input
Lateral amygdala receives sensations slowly from sensory cortex and fast from thalamus, and receives memories from medial temporal lobe. Central amygdala receives from lateral amygdala, prefrontal cortex, and basal amygdala. Basal amygdala receives from lateral amygdala, medial temporal lobe, and prefrontal cortex.
output
Amygdala dopamine neurons connect to cholinergic neurons in medial septal nucleus, nucleus accumbens, nucleus basalis magnocellularis, nucleus of diagonal band of Broca, hypothalamus regions for motivation and reward, and sense and motor cerebral cortex upper layers.
Amygdala sends to orbitofrontal prefrontal cortex, mediodorsal thalamic nucleus, and hippocampal formation.
Lateral amygdala sends to central amygdala. Central amygdala sends to lateral hypothalamus for blood pressure, paraventricular hypothalamus for hormones, motor cortex for stopping, and basal amygdala. Basal amygdala sends to central amygdala.
functions
Amygdala compares new stimulus to previous stimuli and signals differences to other brain regions. Using memory, amygdala participates in habituation and anticipation.
Amygdala {basolateral nucleus} affects aggression, dominance, submission, and territoriality behaviors. Amygdala regulates fear and emotional behavior. Amygdala regulates visceral activity. Amygdala affects vision and smell.
damage
Removal of, or injury to, amygdala does not affect memory.
drug
Cocaine affects sublenticular extended amygdala.
Medulla ganglia {basal ganglia}| include amygdala, caudate nucleus, claustrum, external-capsule fibers, globus pallidus, internal-capsule fibers, lentiform nucleus, nucleus basalis of Meynert, nucleus dorsalis, putamen, septal nuclei, substantia nigra pars reticulata, and subthalamic nucleus.
input
Basal ganglia receive from basal-midbrain-nuclei dopaminergic neurons.
output
Basal-ganglia cholinergic neurons send to motor cortex for transmission to muscles [Langston and Palfreman, 1995].
functions
Basal ganglia assemble, select, and trigger automatic movements, perceptual motor coordination, ballistic movements, and proprioceptively controlled movements, using movement plans. They track moving visual objects, control eye movements, and process visual and multisensory data. They control tremor and muscle tone. Basal ganglia coordinate with neocortex and cerebellum for posture and complex voluntary movements.
Medulla basal ganglia {caudate nucleus} can inhibit globus pallidus. Caudate nucleus receives excitatory input from cerebral cortex and inhibitory input from thalamus, substantia nigra, and raphe. Caudate nucleus is for memory and obsessive behavior.
Medulla basal ganglia {claustrum} can lie under cerebral cortex near insula and project to many cortex regions.
Putamen and globus pallidus {lenticular nuclei} look striated because they have myelinated tracts.
Brainstem regions {motor reticular formation} can facilitate spinal mediated reflexes and transmit feedback from higher centers to primary receptors.
Basal ganglia nuclei {nucleus basalis of Meynert} {nuclei of Meynert} {Meynert nuclei} {substantia innominata} can have cholinergic neurons and send to cerebral cortex.
Basal ganglia nucleus {nucleus dorsalis} receives proprioception input from spinal cord.
Brainstem regions {globus pallidus} {pallidum} can receive from red nucleus and inhibit thalamus and subthalamic nucleus. Dopamine neurons can cause rigidity if overstimulated. Choline neurons can cause hyperkinesis, chorea, and athetosis if overstimulated.
Basal ganglia connect to thalamus, then to cortex, then back to basal ganglia {polysynaptic loop}.
Medulla basal ganglia {putamen} can receive excitatory input from cerebral cortex and inhibitory input from thalamus, substantia nigra, and raphé nucleus. It inhibits globus pallidus. Putamen is for memory, motor skill, and obsessiveness. It has nearby-space maps, used in motor control.
Brainstem regions {raphé dorsalis} can send motor input to superior colliculi.
Medulla nuclei {raphé nuclei} can secrete serotonin, make peptide substance P, start light sleep, and modulate pain, using spinal-cord dorsal-horn presynaptic inhibition.
Forebrain basal ganglia {septal nuclei} {septum, medulla} can receive from hippocampus and reticular formation and send to hippocampus, hypothalamus, and midbrain. Septal nuclei have trophotropic centers. They can control aggressiveness. They organize sexual thoughts, emotions, and action. They are in or near region that causes pleasure when excited.
Putamen, globus pallidus, and caudate nucleus {corpus striatum} {striatum} are near thalamus. They look striated because they have myelinated tracts.
no layers
Corpus striatum neuron types mix but not in layers.
maps
Most maps in mammalian cortex connect to maps in corpus striatum.
functions
Corpus striatum integrates learned automatic movement sequences, such as voluntary eye movements.
input
Some striatum neurons receive from thousands of cortical neurons that send 10-Hz to 40-Hz oscillating signals {interval timer}. Stimuli synchronize oscillations. Oscillators then go on oscillating. Second stimuli make substantia nigra send dopamine to striatum. Striatum remembers signal pattern. If starting signal repeats, dopamine repeats.
output
If pattern matches, striatum signals to thalamus, which informs cortex.
Medulla regions {respiratory center} can send excitatory signals along phrenic nerve to diaphragm.
Nuclei {subthalamic nucleus} {Luys nucleus} {Luys body} {nucleus of Luys} {body of Luys} can be near hypothalamus, inhibit globus pallidus, and send to thalamus. Damage causes ballistic movement.
Fiber bridge {pons}| from hindbrain side to opposite cerebellum side holds major nerve tracts connecting cerebellum and cortex, in both directions, and connects thalamus to olive. Cerebral cortex motor regions influence pons. Pons controls heart, lungs, eye movements, muscle tone, walking, and running. It mediates protective and orientation reflexes.
A pons region {locus coeruleus}| can receive feedback from sense cortex and send to spinal cord, hypothalamus, tractus solitarius nucleus, sensory cerebral cortex, and cerebellum Purkinje cells [Foote and Morrison, 1987] [Foote et al., 1980] [Hobson, 1999]. Locus coeruleus contains few thousand neurons and is largest noradrenaline nucleus.
transmitters
Locus-coeruleus neurons contain neuropeptide Y (NPY) and galanin peptide transmitters.
functions
Locus coeruleus suppresses tonic vegetative regions. It regulates attention, pleasure, energy, motivation, and arousal. It causes deep sleep. REM sleep, cataplexy, grooming, and feeding depress it. Interruptions and multimodal somatosensory stimuli, including pain, excite it. Locus-coeruleus electrical stimulation causes fear and anxiety.
A pons region {pneumotaxic center} receives from nerves that sense alveoli stretching and inhibits breathing.
A pons regions {tegmentum} can include reticular formation and be for attention.
Midbrain ganglia {cuneate nuclei} can receive texture, form, and vibration information in medulla ipsilateral cuneate tracts and send to thalamus, cerebrum, and cerebellum. Maps are smaller than in other areas.
Midbrain nuclei {gracile nuclei} can receive texture, form, and vibration information in medulla ipsilateral gracile tracts and send to thalamus, cerebrum, and cerebellum. Maps are smaller than in other areas.
Midbrain nuclei {inferior colliculi} can send to superior colliculi. They have auditory functions and control eye movements.
Brainstem regions {inferior olive} (IO) can send to cerebellar Purkinje cells.
Midbrain striatum nucleus {nucleus accumbens} receives excitatory dopaminergic pathway from frontal lobes and ventral tegmentum and receives from basal and lateral amygdala. It sends to ventral pallidum. Nucleus accumbens mediates emotions and movements. Benzodiazepine anti-anxiety agent and antipsychotic agents block dopaminergic pathway activation. Regular drug use and other reward stimuli increase delta FosB transcription factor, which causes sensitization and degrades slowly, in nucleus accumbens.
Vertebrates other than mammals have vision cell layer {optic tectum} over large ventricle. Mammals have superior colliculi instead. In amphibia and fish, fibers from retina to tectum keep growing and changing. Mostly unimodal sense pathways go from cerebral cortex to tectum. Tectum makes eye saccades to focus attention-getting object on fovea. Divergence in individual tectum-nuclei loops explains how large recruited tectum-neuron population can form composite command observed at tectum.
Posterior upper brainstem region {parabrachial nuclei} (PBN) receives from sensory trigeminal nucleus and nucleus tractus solitarius and sends motor input to superior colliculi and motor output to hypothalamus and ventral medial basal thalamus.
Pons and thalamus nucleus {periaqueductal gray} (PAG) has opiate receptors and makes endorphins.
Brainstem nucleus {periolivary nucleus} near olive sends to superior colliculi.
Brainstem regions {posterior upper brainstem} can contain periaqueductal gray, parabrachial nucleus, monoamine nuclei, and acetylcholine nuclei. Damage to posterior upper brainstem causes coma.
Brainstem regions {quadrigeminal plate} can have superior and inferior colliculi.
Brainstem nucleus {red nucleus} {ruber nucleus} receives from amygdala and sends to hypothalamus paraventricular nucleus {stria terminalis}. It works similarly to motor cortex.
Brainstem regions {substantia nigra} {substantia nigra pars reticulata} can send to superior colliculus to control eye movement. Substantia nigra cholinergic neurons connect to sense and motor neurons in caudate nucleus and putamen in basal ganglia. Basal ganglia and other midbrain dopamine neurons inhibit caudate nucleus, corpus striatum, and thalamus to coordinate motor function and automatic movement. Alzheimer's disease degenerates substantia nigra neurons.
Mammal midbrain dorsal surface has large symmetrical bumps {superior colliculi} that mediate light accommodation, eyeball movements, body movements for vision, orientation, and attention [Aldrich et al., 1987] [Brindley et al., 1969] [Celesia et al., 1991].
anatomy
Superior colliculus has seven alternating cellular and fibrous layers with few interneurons, eight types of synaptic terminals, and broad dendrite arbors. Superficial layers I to III and deep layers IV to VII have topographic motor maps and associated visual and touch maps.
Superior colliculus removal causes failure to detect contralateral visual stimuli.
anatomy: input
Superior colliculus efferent neurons for eye movements receive input from substantia nigra.
Superior colliculus deep layers receive vision information ipsilaterally from lateral suprasylvian visual area and anterior ectosylvian visual area, not from striate visual cortex.
Deep layers receive somatosensory input from anterior ectosylvian sulcus dorsal part, contralateral sensory trigeminal complex, dorsal column nuclei, lateral cervical nucleus, and spinal cord. Contralateral sensory trigeminal complex receives C fibers and A-delta fibers.
Deep layers receive auditory input from anterior ectosylvian sulcus Field AES region, inferior colliculus contralateral brachium, inferior colliculus external nucleus, nucleus sagulum, and dorsomedial periolivary nucleus.
Deep layers receive motor input from frontal eye fields, motor cortex, zona incerta, thalamus reticular nucleus, posterior commissure nucleus, perihypoglossal nucleus, contralateral superior colliculus, locus coeruleus, raphé dorsalis, parabrachial nuclei, reticular formation, and hypothalamus.
Deep layers receive from basal ganglia through substantia nigra pars reticulata. Deep layers receive from cerebellum deep nuclei, including medial and posterior interposed nuclei.
anatomy: output
Superior colliculus deep layers send to thalamus, opposite superior colliculus, brainstem, and spinal cord. Superior colliculus deep layers connect to sense and motor cerebral cortex and to brainstem and spinal cord, to position peripheral sense organs. Deep layers also send contralaterally to tegmentum and spinal cord to reposition eyes, head, limbs, ears, and whiskers.
neurons: receptive field
Superior-colliculus neurons have central ON zones surrounded by lower sensitivity areas, not like retina and lateral-geniculate-nucleus ON-center-neuron or OFF-center-neuron receptive fields. Receptive fields are larger than in lateral geniculate or cortex neurons. Border is inhibitory {suppressive zone}. The most-effective stimulus is smaller than receptive field. Moving or flashing stimuli are more effective than stationary ones. Movement direction is more effective. Slow movements are more effective than rapid ones. Repeating same stimulus produces response habituation.
neurons: noxious
Superior colliculus neurons {nociceptive-specific neuron} (NS) can respond to noxious stimuli. Superior colliculus neurons {wide dynamic range neuron} (WDR) can respond to all mechanical stimuli, but especially to noxious mechanical or thermal stimuli.
neurons: multisensory
Superior colliculus neurons are 25% unimodal and 75% multisensory. Multisensory and unimodal neurons typically require 100 milliseconds to process information, but some multisensory neurons take 1500 milliseconds.
neurons: auditory
Superior colliculus has four auditory neuron types. Compared to cortical auditory neurons, superior colliculus auditory neurons are more insensitive to pure tones and more sensitive to spatial location, interaural time, and intensity differences. They respond better to moving stimuli, have directional selectivity, habituate to repeated stimuli, and have restricted receptive fields with maximal-response regions.
neurons: somatosensory
Superior colliculus somatosensory neurons respond to hair or skin stimulation, have well-defined receptive fields, prefer intermediate-velocity or high-velocity stimuli, habituate rapidly, are large, have best regions, have no inhibitory surrounding areas, and have no directional selectivity.
neurons: movement field
Midbrain neuron receptive fields {movement field} are like sense-neuron receptive fields. Neurons with similar movement fields are in same superior colliculus region. If neuron activity exceeds threshold, amount above threshold determines saccade movement velocity and distance.
eye movement
Mammal superior colliculi and non-mammal optic tectum process multisensory information, shift attention, and control voluntary and involuntary eye and other sense-organ movements, for orientation and attention. Stimulation shifts eyes, ears, and head to focus on stimulus location. High intensity causes withdrawal or escape.
Anteromedial superior colliculi stimulation causes contralateral, upward, and parallel conjugate eye movement.
Lateral superior colliculi stimulation causes conjugate, contralateral, and downward movement.
To initiate eye movement to periphery, caudal superior colliculus, which represents peripheral visual space, has pre-motor activity.
Visual fixation involves neurons in rostral superior colliculus.
eye movement: saccade
Superior colliculus neurons {motor error neuron} can generate low-frequency, long-duration discharge to signal difference between current eye position and target position. Superior colliculus neurons can initiate saccades and determine speed, direction, and amplitude [Corbetta, 1998] [Schall, 1991] [Schiller and Chou, 1998]. Saccade initiation and velocity, duration, and direction specification are separate processes. Saccade commands are many-neuron vector sums.
Brainstem regions {superior olive} can measure time and intensity differences to differentiate auditory-signal arrival times. Olive sides {lateral superior olive} (LSO) receive inputs from both ears for intensity-level-difference detection. Olive middle {medial superior olive} (MSO) receives inputs from both ears, for time-difference detection. Neurons have time-difference ranges.
Brainstem region {ventral tegmentum} {ventral tegmental area} (VTA) is for pleasure and motivation. Dopamine neurons inhibit nucleus accumbens, mesolimbic system, frontal cortex, and sensorimotor cortex.
Cerebellar cortex {cerebellum}| is for smooth, continuous, and rapid movement. Cerebellar activity is never conscious. Peripheral vision, cerebellum, and vestibular system find body positions.
functions
Cerebellum maintains balance, posture, equilibrium, and muscle tone. It sets appropriate voluntary-muscle motor control, rates, forces compared to resistance, movement directions, and coordination.
functions: comparator
Cerebellum works as comparator. Motor cortex sends to spinal cord to initiate voluntary actions and to cerebellum to inform about intended movements. Proprioceptive nerve input goes to cerebral cortex and then to cerebellum to report actual movements. Cerebellum sends to motor cortex and spinal cord to correct movements.
functions: damping
Damping involves inhibiting agonist and antagonist contractions to eliminate muscle tremor, for smooth movement.
functions: error control
Error control involves initial strong muscle contraction and subsequent antagonist-muscle contraction.
functions: feedforward
Sense delays prevent feedback alone from controlling fast and accurate biological movements. Cerebellum uses predictive, feedforward control.
functions: gain
Perhaps, cerebellum controls amplification gain in spinal and brainstem reflexes. Cerebellum can subtract adjustable signal from fixed-gain saccadic circuit.
functions: precision
Cerebellum compares sense stimuli about actual performance with movement program received from cerebrum, measures error, and corrects movement. For example, it regulates smooth eye movements by tuning reflexes using Purkinje cells.
It regulates premotor networks by inhibiting and disinhibiting motor-control actions that begin in brainstem, sensorimotor-cortex, and spinal-cord premotor networks. To control movement, Purkinje cells first exert increased inhibition on deep nuclei excited by cerebral cortex and sense information. Then, inhibition decreases, and deep nuclei send excitatory output to pons and red nuclei, which send to motor cortex.
functions: prediction
Prediction involves comparing information received from eyes, body, and cerebrum, to calculate when to slow and/or stop motion.
functions: progression
Progression involves muscle contraction in sequence, to coordinate and time.
functions: sensation
Cerebellum coordinates information from different senses. Skin touch receptors send to separate cerebellum areas. Cerebellum reacts more quickly to auditory stimulus than visual stimulus. Cerebellum reacts faster to higher intensity and multiple sensory stimuli.
Cerebellum affects sense accuracy, sense quickness, sense timing, short-term memory, attention, emotions, and planning. Lateral cerebellum affects perception, pattern recognition, and cognition.
functions: timing
Perhaps, cerebellum is for timing. Perhaps, parallel fibers are delay lines, and climbing fibers are clock read-out mechanisms. When parallel fiber and climbing fiber activation coincide, Purkinje cells fire to activate antagonist muscles and stop movements at intended targets.
One climbing fiber synapses on one Purkinje cell. Perhaps, cerebellar clock activates proper Purkinje-cell assemblies at right time.
learning
Cerebellum learns movement timing and guides learning in deep nuclei. It stores learned-skill model or memory within six hours, so skill becomes automatic.
learning: long-term depression
Increased dendritic calcium concentration induces cerebellar long-term depression (LTD). Cerebellar LTD reduces excitatory input to Purkinje cell. LTD can decrease synaptic weights, using climbing fiber input as training signals, Purkinje cell firing as postsynaptic factor, and/or parallel fiber synaptic activity as presynaptic factor. LTD at basket-cell and stellate-cell spiny synapses maintain excitatory input to Purkinje cells [Eccles et al., 1976].
cells: basket cell
Basket cells lie in Purkinje cell dendrites.
cells: flocculus neuron
Flocculus neurons send corrective signals for movements.
cells: Golgi cell
Golgi cells lie in middle layer between Purkinje cells.
cells: granule cell and parallel fiber
Granule cells are small neurons, have high density, and are the most common. Granule-cell-axon parallel fibers pass through middle layer, contacting one Purkinje cell many times, to outer layer, where they split, form straight line, and extend horizontally through outer layer. Parallel fiber is perpendicular to hundreds of Purkinje cell dendrite trees and contacts each once.
cells: Purkinje cell
Purkinje cells are large neurons that have tree-shaped flat dendrite planes, which converge onto one trunk into Purkinje cell. Purkinje cell membrane has 150,000 synapses, ten times more than other neuron types, mostly from granule cells. Purkinje cell axons inhibit Golgi cells and granule cells in cerebellar nuclei, which send axons to brain pyramidal and extrapyramidal tracts.
cells: stellate cell
Stellate cells lie beside Purkinje cell dendrites and have fibers that run horizontally through outer layer, mainly through one Purkinje cell dendrite tree.
biology
Cerebellum anatomy is the same in all vertebrates. Cerebellum has surface area equal to one cerebral hemisphere. It has more than half of all brain neurons. It has more folding than cerebrum.
Low-threshold cerebellar receptive fields and neurons align with nociceptive punishment signal fields and neurons.
biology: damage
Cerebellum damage decreases muscle tone, causes slowing and trembling, and fails to stop movements on time. One-side damage causes flexion on one side and extension on other. Within 45 minutes, cutting spinal cord stops flexions and extensions. Cutting after 45 minutes does not stop flexions and extensions. Cerebellum damage in early life does not affect behavior.
biology: evolution
During human evolution, cerebellum expanded at same rate as cerebrum.
biology: input
Sensory cerebellum receives tactile, visual, and auditory nerves. Cerebellum lobes have body-surface tactile representations.
biology: output
Motor cerebellum has reverberatory circuit to higher motor centers, regulates voluntary movements, organizes somatotopically, and has archicerebellum and neocerebellum. Motor cerebellum maintains muscle tonus, posture, and equilibrium.
biology: waves
Cerebellum has electrical waves lasting 150 to 200 milliseconds, at 0.02 mV to 0.12 mV.
biology: layers
Inner deep granule-cell layer has closely packed granule cells, as well as scattered Golgi cells that inhibit nearby granule cells. Middle Purkinje-cell layer has one Purkinje-cell row, surrounded by smaller basket cells. Wide outer-molecular layer has Purkinje cell dendrites that spread in plane and stellate cells that contact dendrites.
biology: pathways
Cerebellum receives excitatory input from vestibular-system mossy fibers or pons climbing fibers. Mossy fibers from vestibular system synapse with Golgi cells and granule cells. Mossy fibers from Golgi cells and granule cells send to Purkinje cells and process intersensory information. Pons climbing fibers synapse with granule, Golgi, Purkinje, basket, and stellate cells. Purkinje cells inhibit Golgi cells and granule cells.
biology: peduncles
Cerebellum attaches to posterior brainstem by three pairs of stalks {cerebellar peduncle}, which contain both afferent and efferent nerve fibers. Superior, middle, and inferior tracts join cerebellum to midbrain. Tract {superior peduncle} comes from neocortex. Tract {middle peduncle} {brachium pontis} comes from pons. Tract {inferior peduncle} comes from inner-ear vestibular apparatus.
biology: hemispheres
Cerebellum has two lateral parts {cerebellar hemisphere}, which have many small folds {folia}, connected by thin central worm-shaped part {vermis}. Vermis has inferior part that controls gross motor coordination and superior part that controls fine motor coordination. Gray-matter outer cover {cerebellar cortex} is over white matter {medullary body}.
biology: nuclei
Four deep nuclei are in cerebellar white matter. All vertebrates have the oldest cerebellum part {archicerebellum} {vestibulocerebellum}, in center {flocculus} {nodule, cerebellum}, which has afferent and efferent connections in inferior peduncle, mainly with inner-ear vestibular semicircular canals {maculae}. Cerebellum has small inferior portion {flocculonodular lobe}, for balance, position, head position changes, acceleration, deceleration, and angular movements. Fibers from retina, eye movement nuclei, and cortex terminate in vestibulocerebellum. The second oldest part {paleocerebellum} {spinocerebellum} corresponds to anterior lobe and posterior vermis and receives touch, pressure, thermal, and proprioceptive input from inferior-peduncle ascending spinal-cord and brainstem pathways. Skin, muscle, and tendon receptors send performance information about rate, force, and movement direction, especially propulsive movements such as walking and swimming.
Perhaps, cerebellum has static associative memories {Cerebellar Model Articulation Controller} (CMAC) that implement locally generalizing non-linear maps between mossy-fiber input and Purkinje-cell output. Granule and Golgi cell-network association layer generates sparse expanded mossy-fiber-input representations. Adjustable weights couple large parallel fiber vector to Purkinje-cell output units with graded properties.
pattern
Adjustable pattern generator (APG) model can generate elemental burst command with adjustable intensity and duration. It models positive feedback between cerebellar nucleus cell and motor cortical cell.
Excitatory input {climbing fiber} from inferior olive goes to one Purkinje cell, making 300 synapses, to fire Purkinje cell. Perhaps, climbing fiber makes error-and-training signals to adjust parallel-fiber synaptic weights, teaching Purkinje cells to recognize patterns signaled by input vectors and to select movements that reduce errors. Perhaps, cerebral cortex activates climbing fiber input, to train cerebellum to recognize appropriate contexts for generating same movements more automatically.
Inferior-olive small neuron clusters, with similar receptive fields, stimulate parasagittally-oriented cerebellar Purkinje-cell strips, which send to cerebellar nuclear-cell common cluster {microzone}.
Spinal-cord and brainstem excitatory axons {mossy fiber} synapse on more than 40 granule-cell glomeruli and deep-cerebellar nuclei. Mossy fiber also directly contacts 250 Purkinje cells but cannot fire them. Mossy fiber influences 200,000 Purkinje cells. Mossy fibers have sensory properties, but Purkinje and nuclear cells do not respond to somatosensory stimulation.
The newest and largest cerebellum part {neocerebellum} {pontocerebellum} is anterior and posterior cerebellar lobes, for skilled or complex movements and intentions. Neocerebellum receives from pons and sends through superior peduncle.
Excitatory axons {parallel fiber} from cerebellum send to Purkinje cell dendrites. Perhaps, parallel fibers provide input vectors. Parallel fibers form sequential-activity lines, with one synapse per Purkinje cell. Parallel fibers can induce long-term depression.
Cerebellum has seven million large neurons {Purkinje cell}, which receive 200,000 synapses on planar dendritic spines and send inhibitory GABA output to cerebellar deep nuclei.
A forebrain region {cerebrum}| {cerebral hemispheres} {cerebral cortex} above midbrain includes telencephalon and diencephalon. Cerebrum initiates behavior, causes consciousness, stores memories, and controls internal stimuli.
size
Human cerebral cortex is 2000 square centimeters in area and 300 cubic centimeters in volume.
neurons
Cerebral cortex has more than one billion neurons. Half are pyramidal cells. Surface folding increases area and density. Cerebrum has 100,000 to 300,000 neurons per cubic millimeter.
parts
Mammal cerebrum includes neocortex and hippocampus.
layers
Mammal cerebral-cortex layers average 2 millimeters thick, differing in thickness among the 52 Brodmann areas. Layers are on outside, with axon fibers on inside. Macrocolumns and their minicolumns go through all layers.
Limbic system typically has three-layered allocortex. Cingulate gyrus and insula have three to six cortex layers in juxtallocortex. Human cerebral hemispheres have six-layered neocortex. Top three layers are only in genus Homo and act as a unit. Cortex has only one inhibitory-cell layer.
layers: general
Layer 1 has horizontal cells. Layer 2 has small, round, granular cells. Layer 3 has pyramidal cells. Layer 4 has closely packed granular cells. Layer 5 has large and numerous pyramidal cells and has large spindle neurons, which begin after birth in anterior cingulate and frontal area FI and are for attention and self-reflection. Layer 6 has spindle-like small cells.
layers: detail
Top layer 1 contains pyramidal cell apical dendrites from other layers in macrocolumn and axons from other cortical areas, with few neuron cell bodies. Layers 2 and 3 have superficial pyramidal cells. Layers 1, 2, and 3 {superficial layers} receive from their column, other cortex, and thalamus matrix neurons. Layer 4 has many excitatory spiny stellate cells but few pyramidal neurons. Layer 4 has sublayers IVa, IVb, IVc, and IVc in visual cortex. Layers 5 and 6 {deep layers} have pyramidal cells, some with dendrites to layer 1, that send to cortex, thalamus, superior colliculus, and spinal cord.
layers: input and output
Layers 1 and 2 and layer-3 upper part receive from other cortical-area layer 4. Layers 1 and 2 and layer-3 upper part send to other cortical-area layer 5. Layer-3 lower part receives from outside cortex and sends to layers 1 and 2 and layer-3 upper part. Layers 2 and 3 mostly connect to layers 2 and 3, either laterally or through U-shaped fibers going down into white matter and then back up. Layers 2 and 3 also send to layer-3 lower part and to layer 4 for feedforward responses. Some layer-2-and-3 superficial neurons send output to layers 5 and 6. Layer 4 receives from layer 6 and from outside cortex. Layer 4 sends mainly to layers 1 and 2 and layer-3 upper part. Layer 5 receives from layers 1 and 2 and layer-3 upper part, from whole cortex. Layer 5 sends to layer 6, spinal cord, brainstem, basal ganglia, and hypothalamus. Layer 5 neurons do not project to other cortical areas, thalamus, or claustrum. Layer 6 receives from layer 5. Some layer-6 neurons receive from layer 4C. Layer 6 sends short vertical axons back to layer 4 and outputs to thalamus. Some layer-6 neurons send to thalamus, lateral geniculate nucleus, and claustrum.
layers: connections
Lateral axons are within all layers. Ascending and descending fibers connect all layers. Adjacent cerebral cortex areas always connect to each other. Distant cortical regions connect reciprocally.
input
Cerebrum receives from higher brainstem and limbic system. Brainstem or limbic system damage reduces cerebrum activity, and people enter dreamy state.
Ascending fibers to cerebral cortex have slow, long lasting NMDA receptors.
Excitatory input comes from ipsilateral cerebral cortex, and inhibitory input comes from contralateral cortex. Cerebral cortex mainly inhibits lower brain. It does not control older brain parts but interacts with them.
Cortical motor areas receive input from association areas, corticospinal tract, thalamus, post-central gyrus somaesthetic area, and frontal lobe motor areas.
input: topography
Cortical neurons separated by less than several hundred microns receive similar input and send similar output.
input: multisensory
Cortical neurons for multisensory information lie next to cortical areas for one sense. Superior-temporal, intraparietal, frontal, and prefrontal lobes are for multisensory convergence [Bruce et al., 1986].
input: synapses
70% of excitatory synapses on cerebral-cortex superficial pyramidal neurons are from less than 0.3 millimeters away. Few come from outside cerebral cortex. Average cortical-neuron effect on other neurons is 0.050 to 5 millivolts. Probability of one synapse causing a spike is 0.1 to 0.5.
Cortical neurons have dendritic trees with diameter 0.3 millimeters. Most neurons receive 100 synapses from 100 neurons and send to 100 other neurons. 8000 neurons eventually affect cortical neurons.
input: processing
Training, learning, and willing have widespread cortical activity and take one second.
Consciousness involves coordinated synchronized impulses in cerebral cortical neurons for over 100 milliseconds. Perhaps, impulses are high-frequency bursts, rate codes, oscillations at 40 Hz, or other synchronized impulses. Visual consciousness involves cortical layers 5 and 6. Cortical layer 4 receives input. Cortical layers 2 and 3 are for unconscious processing.
output
Motor and sense cortex sends axons to cerebellum, basal ganglia, and hippocampus, which send axons to thalamus and cortex, with no reciprocity.
Cerebral-cortex descending fibers can cause lower-brain-neuron long lasting subthreshold depolarization.
Cerebrum primary sense areas send to nearby secondary areas and nowhere else. Secondary sense areas send to other-hemisphere corresponding area, other same-hemisphere secondary areas, and cerebral association areas. Association areas interconnect.
output: synchronization
Cerebral-cortex superficial-pyramidal-cell axons travel horizontally in same cortical layer 0.4 to 0.9 millimeters and then make terminal clusters on other superficial pyramidal cells. The skipping pattern aids neuron-activity synchronization.
output: divergence
As signal travels farther into cerebrum, neuron receptive-field sizes increase and features to which neurons respond become more complex, because later areas receive input from several earlier areas.
output: feedback
Later areas send signals back to earlier areas.
damage
People with no cerebrum can sleep, awake, smile, and cry. They feel no danger or hunger and have no spontaneous behavior.
Damage to cortex causes poor memory retrieval and poor habit inhibition. Cortex loss does not affect general consciousness.
Limbic system cortex {allocortex} {archicortex} typically has three layers.
Cortical regions {association cortex} can record pattern and feature shapes, sizes, types, strengths, and indexes. Association cortex uses serial and parallel detectors at sensory field points to find perceptual features and associate them with similar patterns.
vector field
Associative cortex receives spatial and temporal chemical and electrical signal-intensity patterns from neuron arrays and then distributes spatial and temporal chemical and electrical signal patterns to neuron arrays, including self. Spatial and temporal pattern is like wave front or vector field. Association cortex transforms, and so maps, input field to output field. Mapping uses tensors. Vector-field output vectors are input-vector functions. Vector fields have gradients, flows, constancies, covariances, and contravariances. For example, before intention to move and before movement begins, non-motor cortex has activity. Brain compensates for body movements that change sensor and muscle positions.
levels
Primary associative cortex tracks interactions, combinations, correlations, constancies, covariances, and contravariances among neural signals.
Secondary associative cortex creates absolute time and space, through body-position and surrounding comparisons, as body, head, and eyes move. Spaces have one, two, two and a half, or three dimensions for different uses. Model locates sense organs and muscles in three-dimensional time and space, as objects where events happen. Three-dimensional space-time does not depend on body and has vertical, front, right, and left. Absolute space-time allows perspective changes and unites perception and action.
Tertiary associative cortex is only in human brain and coordinates intermodal sense information.
Rodent somatosensory-cortex regions {barrel field} can be for sensations from same-side whiskers (Thomas Woolsey and Hendrik van der Loos) [1975]. Neuron groups {barrel, neuron} can respond first for one whisker, respond later for nearby whiskers, and respond even later for farther whiskers. Barrels feed back to previous barrels. Thalamus also has barrel-like regions {barreloid}. Brain stem has barrel-like regions {barrelet}.
Passive signal reception has refractory periods, but active exploration has no refractory periods. Active exploration has priming.
Brain hemispheres have 52 regions {Brodmann area}, classified by cortical-layer thickness. Average human Brodmann area is two square inches. Brodmann areas can have one to six distinct physiological subregions, each one-centimeter square. For example, area 17 has one map.
A cleft {central fissure} {central sulcus} {rolandic sulcus} lies between pre-central gyrus and post-central gyrus.
Humans perform some mental functions predominantly in left or right cerebrum {cerebral dominance}.
Cortex folds on itself {convolution, cortex}| in set patterns.
From corpus callosum to gray matter {cingulum} are myelinated axons.
In placental mammals, 800 million axons {corpus callosum}| connect left and right cerebral hemispheres [Aboitiz et al., 1992] [Kretchmann and Weinrich, 1992].
Brain also has smaller connections between hemispheres.
processing
Corpus-callosum posterior splenium relays visual information from left visual field to speech area.
damage
Cutting corpus callosum causes epileptic-like brain firing.
split brain
Cutting all connections between left and right hemispheres can show psychological functions performed by hemispheres. Cutting only corpus callosum makes no change, because other connections can still carry signals.
After cutting, people cannot match unseen object felt by the hand to seen object felt by right hand. Two separate experiences or discriminations can happen simultaneously.
Both hemispheres know words, pictures, and metaphorical relationships. Both hemispheres are aware.
Will, consciousness, motivation, and coordination are only slightly depressed, except for short concentration lapses. Perception, object location, and space orientation stay the same.
Either hemisphere can activate, depending on task, sex, age, handedness, education, and training.
Over time, functions performed by hemispheres become more alike.
brainstem
Brainstem dismay, embarrassment, or amusement feelings, generated in one hemisphere by threat, risk, or teasing perceptions, can cause body movements, emotions, attention, and orientation.
Mammal neocortex cerebral hemispheres {isocortex} can have six layers.
Cingulate gyrus and insula {juxtallocortex} have three to six cortex layers.
A brain hemisphere {left hemisphere}| stores categorical relationships and organizes movements in right limbs.
functions
It has region, between occipital, parietal, and temporal lobes, for mathematical thinking. It is better at propositional speech. It predicts how words will sound. It stores learned skills. It directs right-hemisphere left-limb control. It has relatively more neurons and fewer axons, so connections are shorter for analyzing details.
damage
Damage to left posterior hemisphere harms language coding. Large damage to left hemisphere causes language ability loss but does not affect automatic language.
Cortex can not fold and is smooth {smooth brain} {lissencephaly}.
Cortex {neocortex}| {new forebrain} can be only in mammals, for sense memory [Abeles, 1991] [Allman, 1998] [Braitenberg and Schüz, 1991] [Braitenberg, 1984] [Felleman and Van Essen, 1991] [Mountcastle, 1957] [Mountcastle, 1998] [Passingham, 1993] [Peters and Rockland, 1994] [Peters et al., 1991] [Rockel et al., 1980] [White, 1989] [Zeki, 1993]. It has uniform neuron structure.
regions
In humans, neocortex has at least 52 distinct cellular areas. Cat neocortex has 36. Rat neocortex has 13. In some primates, striate cortex differs from motor cortex, with giant Betz cells, in laminar organization, cell number, cell types, and general connectivity patterns.
Upper-temporal-lobe region {planum temporale} controls complex movements and language processing.
Nuclei {precuneus} can be about autobiographical memory.
Sense neurons have spatial regions {receptive field} from which stimuli can come [Kuffler, 1952] [Ratliff and Hartline, 1959]. Retinal neurons have receptive fields with center circle and surrounding annulus with opposite polarities {center-surround organization}.
Vision has topographic maps {retinotopic map}, in which fovea has more points than surround.
Hemispheres {right hemisphere}| can have relatively fewer neurons and more axons, so connections are longer. It can recognize larger patterns. It has region, between occipital, parietal, and temporal lobes, for spatial thinking. It analyzes visual and spatial relations. It gives direction sense. It can perceive shapes by touch. It recognizes faces. It understands interpersonal acts. It does more distance judging. It judges temporal order such as simultaneity and time differences. It synthesizes whole situation to develop emotional response.
language
Right hemisphere cannot express speech but can comprehend spoken and written language. It can judge word meaning from sound but cannot make sound from visual image. It comprehends all grammatical word classes, except difficult, abstract, or rare words. It cannot comprehend proposition. It cannot group using tokens. It is better at automatic speech and skilled motor acts. It can solve simple arithmetic problems.
music
Right hemisphere is for intonation, background noise elimination, music, and chords.
Ventrobasal thalamus and ventral tegmentum dopaminergic neurons stimulate cerebrum {sensorimotor cerebral cortex}.
Cerebral hemisphere posterior parts {sensory cortex} receive, preserve, and elaborate information from external world. Three million sense-neuron axons go to cerebral cortex.
Cortex regions {somaesthetic cortex} can be for touch, have double body-surface representation, depending on number of surface skin receptors, and discriminate among touch sensations.
Cortex regions {somatosensory cortex} can receive touch information from thalamic-relay nucleus on somatosensory area 1 {area S1}, which sends to somatosensory area 2 {area S2}. Attention affects somatosensory cortex [Steinmetz et al., 2000].
Brain has touch topographic map {somatotopic map} {somatosensory map} behind central fissure. Largest areas are for body regions used most frequently for tactile orientation and analysis, such as face, forepaw, and forelimb. Somatotopical and visual body-surface representation is upside down in vertebrate brains. Somatosensory-map hand region changes size, if hand exercises more. Body-movement topographic map in front of central fissure aligns with somatosensory map.
A cleft {lateral fissure} {sylvian fissure}| is between temporal lobe and parietal lobe.
Brain color-processing regions {TPO region} {temporal parietal occipital region} can be at temporal-lobe, parietal-lobe, and occipital-lobe junction near angular gyrus. It also represents sequences and order. It connects touch, hearing, and vision. Perhaps, left side is multisensory, and right is spatial [Ramachandran, 2004]. TPO region expanded greatly from mammals to humans. Perhaps, it is for moving in trees as hands grasp branches.
Brain has two-dimensional neuron arrays {topographical mapping} {topographic map, brain}| for analysis [DeYoe et al., 1996] [Dow, 2002] [Hübener et al., 1997] [Horton and Hoyt, 1991] [Swindale, 2000] [Tootell et al., 1998] [Van Essen et al., 2001].
locations
Vision has topographic maps in retina, lateral geniculate nuclei, area V1, and area V2, for analyzing color, movement, disparity, orientation, size, and spatial periodicity. Audition has at least six topographic maps in primary auditory cortex and surrounding cortex, for analyzing tones and locations. Touch has at least four topographic maps in somatosensory cortex and surrounding cortex, for analyzing surface texture and shape. Proprioception has at least four topographic maps, for analyzing muscle stretching, compressing, and twisting.
Motor control also uses at least four topographical maps.
Sense and motor maps align and connect. Brain maps in different brain areas are not homogeneous and not isotropic.
layers
Maps can have neuron layers.
processing
Neurons that process signals from neighboring positions or times are near each other.
processing: number
Neuron number is proportional to processing amount. In touch maps, hand has more neurons and larger area than back. In retinotopic maps, fovea has more neurons and larger area than whole surround.
processing: inhibition
Connections within map are mostly inhibitory. Lateral inhibition enhances contrast and suppresses noise.
Topographic maps with diffuse connections and large receptive fields are beside maps with specific connections and small receptive fields, so map sets work at different spatial and temporal scales.
processing: filling-in
Maps can extrapolate and interpolate.
processing: space
Coordination among two-dimensional topological maps allows two-and-a-half-dimensional and three-dimensional representations.
In visual cortex, columns {hypercolumn} of 100 cells, one millimeter diameter, can detect stimuli from one spot in visual field, from both eyes. Hypercolumn can detect orientation, from 0 to 180 degrees, and depth, and so perspective, size, shape, and surfaces. Hypercolumn macrocolumns can receive from left or right eye. Hypercolumn cells use several visual-field region sizes. Cells can be simple, complex, and hypercomplex.
Neuron columns {macrocolumn} can share functional properties for one body-surface patch [Buxhoeveden and Casanova, 2002] [Koulakov and Chklovskii, 2001] [Mountcastle, 1957] [Mountcastle, 1998] [Rakic, 1995].
properties
Macrocolumn is 0.4 to 1.0 millimeters diameter. It goes through all six cortical layers. It has 100 minicolumns. It is plastic.
bands
It makes interdigitating curved planes. Somatosensory neurons responsive to skin stimulation alternate with neurons for joint and muscle receptors, every 0.5 millimeters. New-World monkeys do not have ocular dominance columns.
cause
Perhaps, self-organizing competition and cooperation, during development and learning, cause macrocolumns.
Macrocolumn units {minicolumn} are in all reptile, bird, and mammal cortex. Column is 23 micrometers to 65 micrometers diameter, thin hair size. It contains 110 to 250 neurons. It organizes around bundle of 12 apical dendrites. It goes through all six cortical layers. It is 30 micrometers apart in human cortex.
processing
Within ocular-dominance macrocolumns, minicolumn orientation columns can prefer lines and edges that tilt same angle from vertical {orientation tuning, minicolumn}. Superficial-layer recurrent excitation coordinates distant minicolumns.
growth
Cortex grows by adding minicolumns, which travel from inside to outside. Perhaps, self-organizing competition and cooperation, during development and learning, cause minicolumns.
Minicolumns {ocular dominance column} can have 3000 input axons and 50,000 output axons. Signals to column from right or left eye ocular dominance process faster. Visual-cortex hypercolumns have equal numbers of both ocular dominance columns [Hubel and Wiesel, 1968] [Hubel, 1988] [Horton and Hedley-Whyte, 1984] [LeVay et al., 1985].
Ocular dominance columns are independent units 0.4 to 0.5 millimeters apart. They have bands for same orientation or same eye.
Ocular dominance columns are only in Old-World monkeys, apes, and humans, and not in New World monkeys.
Minicolumns {orientation column} can have 3000 input axons and 50,000 output axons [Blasdel and Lund, 1983] [Blasdel, 1992] [Das and Gilbert, 1997] [LeVay and Nelson, 1991]. Orientation column is an independent unit. It has 120 cells, all for one orientation. Columns are 0.4 to 0.5 millimeters apart.
bands
Columns have bands for same orientation or same eye.
functions
Cells can detect stationary objects at locations. Cells for larger areas can check for movement and flashing, often from one direction only. Cells can check for corners, lengths, and trajectories. Orientation columns can extract contours, as curve envelopes, or can output cell-signal mean values, most-active-neuron signals, or pulse patterns.
Diencephalon nerve-fiber band {fornix} connects amygdala and hippocampus to septum, preoptic area, and hypothalamus.
Nuclei {epithalamic nuclei} near thalamus include habenular nuclei, pineal gland, and habenular commissure.
Fibers {habenular commissure} connect habenular nuclei in epithalamus.
Epithalamic nuclei {habenular nuclei} can receive from thalamus.
Foremost ventral brainstem {hypothalamus, brain}| connects to limbic system within temporal lobe.
input
Hypothalamus receives excitation and inhibition from non-sense and non-motor cortex that organizes emotions and behavior.
output
Hypothalamus has dopaminergic nuclei, cholinergic nuclei, and histaminergic nuclei that project in net over whole brain.
Hypothalamus makes orexin, which goes to lateral-hypothalamus receptors.
hormones
Hypothalamus parvocellular neurons respond to adrenal glucocorticoid hormones to decrease corticotrophin-releasing-factor production.
Hypothalamus sends to gland regulators to control hormone production and sends to sympathetic and parasympathetic nervous systems.
nuclei
Hypothalamic nuclei include arcuate, dorsomedial, mamillary, paraventricular, optic chiasm, preoptic, posterior, suprachiasmic, supraoptic, tuber cinereum, and ventromedial nuclei. Sensory hypothalamus has mamillary bodies. Ergotropic centers are in hypothalamus posterior. Trophotropic centers are in hypothalamus rostral part, septum, and preoptic region.
functions
Hypothalamus is for aggression, submission, fighting, flight, rage, attention, aversion, and fear.
It is for sex behavior and sex inhibition, using sex hormone receptors. It organizes copulation in front hypothalamus and septal area.
It is for appetite, eating, digestion, micturition, and defecation. It organizes body metabolism, heat production, body temperature, and circulation.
Hypothalamus is for repose, sleep, and wakefulness. Sensory hypothalamus carries wakefulness impulses from reticular formation to thalamus.
Hypothalamus does not initiate behavior.
evolution
At first-ventricle bottom, chordates had secretory cells that evolved to make hypothalamus.
Hypothalamus regions {arcuate nucleus} can have main proopiomelanocortin (POMC) neurons and send to limbic system and brainstem. POMC is precursor of MSH.
processing
Arcuate nucleus has region for appetite and region for satiation. Ghrelin gut peptide stimulates appetite region. PYY gut peptide inhibits appetite region. Leptin hormone stimulates satiation region and inhibits appetite region. Insulin hormone stimulates satiation region and inhibits appetite region. Satiety region sends alpha-MSH to MC4 second-satiation-region receptors. Appetite region sends AgRP to second satiety region, neuropeptide Y (NPY) to second appetite region, and melanin concentrating hormone (MCH) peptide.
hypothalamus region {dentate gyrus}.
Hypothalamic ganglia {dorsomedial hypothalamic nucleus} can be for ejaculation.
Hypothalamic nuclei {lateral hypothalamic nucleus} can be for hunger.
Hypothalamus nuclei {mamillary bodies} can be for long-term memory.
Hypothalamus regions {motor hypothalamus} can be main below-cortex limbic-system part, control reflex pupil dilation, and integrate autonomic nervous system, together with old cortex. Fore part is for parasympathetic nerves. Back part is for sympathetic nerves. It has richest blood supply, reciprocally connects blood vessels to pituitary gland, and regulates pituitary-hormone secretions.
functions
It affects homeostasis, regulates body temperature, regulates water metabolism and excretion, and regulates food intake. It makes overall sexual behavior pattern and has pleasure center related to sex behavior.
Hypothalamic nucleus {paraventricular nucleus} receives from amygdala and sends to posterior pituitary.
Tuberal region has nucleus {posterior hypothalamic nucleus}, beside arcuate nucleus, that connects with lateral mamillary nucleus.
Hypothalamic nuclei {preoptic nucleus} can have trophotropic centers. Medial preoptic area is about maternal behavior.
Light on retina signals optic-nerve retinohypothalamic tract, which signals hypothalamus nuclei {suprachiasmic nucleus} {suprachiasmatic nucleus} (SCN), which causes daytime pineal-gland melatonin-production reduction by inhibiting paraventricular nuclei.
Hypothalamic nuclei {supraoptic nuclei} can project to posterior pituitary.
hypothalamic nucleus {tuber cinereum}.
Hypothalamic nuclei {ventromedial hypothalamic nucleus} can be for satiation.
Above hypothalamus is golf-ball-sized ellipsoidal region {thalamus}|.
functions
Thalamus is for attention, respiration, short-term memory, and long-term memory. It can detect sensations, temperature, pain, and moderate skin stimulation. It identifies objects and initiates avoidance behavior. In mammals and humans, it directs attention to language. It affects autonomic system.
Thalamus has feeding center that controls eating behavior. It has satiety center that has glucose receptors.
anatomy
Ventral reticular nucleus is thin shell that surrounds walnut-sized dorsal thalamus. Thalamus has few intrinsic neurons.
anatomy: nuclei
Thalamic nuclei include anterior, centromedian, dorsolateral, dorsomedial, intralaminar, lateral geniculate for vision, medial geniculate for audition, multimodal, pulvinar, reticular, ventral anterior, ventral lateral, ventral posterior, and ventrobasal complex for somatosensation [Jones and Peters, 1986] [Jones, 1985] [Sherman and Guillery, 2001].
input
Main inputs to cortex first pass through two dozen thalamus regions. Glomeruli and glia surround incoming sense-nerve axons. Thalamus has projection areas for skin regions, with subareas for touch, pressure, muscle, and joint movement. Thalamus has input neurons for taste and for taste and touch.
Number of cortical fibers projecting back to thalamic nuclei is much larger than number of fibers from senses to thalamus.
output
All nuclei have matrix cells with diffuse projections. Thalamus has as many outputs as inputs but has no axon collaterals.
Thalamus inhibits optic tectum in lower vertebrates.
Core relay neurons send to cortex layer 4. Matrix neurons send to cortex layers 1, 2, and 3. Clustered neurons {core neuron}, such as magnocellular and parvocellular neurons, excite layer 4 in small cortex regions. Other neurons, such as koniocellular neurons, send to layers 2 and 3 in larger cortical regions {matrix neuron} [Jones, 2002].
damage
Non-specific thalamus damage causes consciousness loss. Thalamic damage can cause sense or motor loss.
processing
Input causes one spike and then 100 milliseconds of inhibition. Thalamic neurons can replicate sense input or can burst in 30-Hz to 40-Hz pattern unrelated to input. Thalamus reticular nucleus can switch lateral geniculate nucleus into burst mode.
Limbic-system anterior-thalamus region {anterior thalamic nucleus} {anterior sensory thalamus} relays affective visceral information to cortex and controls ergotropic behavior through sympathetic nervous system.
Thalamic nucleus {centromedian nucleus} {centrum medianum nucleus} sends to cerebellum and corpus striatum.
Thalamic ganglia {dorsolateral thalamic nucleus} can send to parietal lobe.
A limbic-system part {dorsomedial thalamic nucleus} can receive from olfactory lobe and amygdala and send to frontal lobe and hypothalamus.
Lateral geniculate nucleus sends, through optic radiation {geniculostriate pathway, brain}, to occipital lobe visual cortex area V1. Geniculostriate and tectopulvinar pathways interact. Lateral geniculate nucleus damage causes poor acuity.
Thalamus medullary-laminae nuclei {intralaminar nuclei} {intralaminar complex} (ILN) {nucleus circularis} can have neurons organized in torus and include geniculate bodies. ILN surrounds medial dorsal nucleus. Other thalamic nuclei are principal nuclei.
purpose
Loops through striatum, pallidum, and thalamus underlie arousal and awareness.
input
Intralaminar nuclei receive from reticular formation for arousal, spinothalamic system for temperature and pain, trigeminal complex for temperature and pain, cerebellum dentate nuclei for proprioception, globus pallidus for motor feedback, periaqueductal gray for emotion, substantia nigra for emotion, amygdala for emotion, and vestibular nuclei for body position.
Laterodorsal tegmentum, peduncle, and pons cholinergic neurons excite excitatory thalamocortical-relay-neuron nicotinic receptors, and those cholinergic neurons inhibit inhibitory thalamic-reticular neuron muscarinic receptors, resulting in new excitation. Basal forebrain cholinergic and noradrenergic axons go to Layer I and to lower layers. Ventrobasal nucleus sends to Layer IV.
output
Intralaminar nuclei connect, with collaterals to nucleus reticularis, to striatum, pulvinar, all cortical layers 1 to 3, except visual cortex and inferotemporal cortex, and basal ganglia.
Intralaminar nucleus {centrum medianum} {entromedian nucleus} stains differently, is for will, and sends to motor cortex and striatum.
Intralaminar-nuclei matrix neurons can send to Layer I, to modulate lower layers. Intralaminar-nuclei core neurons can send mainly to Layer V and VI, to carry main signals.
damage
Strokes in thalamoperforating arteries {paramedian arteries} can damage both ILN. Both-side damage ends waking consciousness [Baars, 1995] [Bogen, 1995] [Cotterill, 1998] [Hunter and Jasper, 1949] [Kinney et al., 1994] [Koch, 1995] [Llinás and Paré, 1991] [Minamimoto and Kimura, 2002] [Newman, 1997] [Purpura and Schiff, 1997] [Schlag and Schlag-Rey, 1984].
Lateral geniculate nucleus has six separate cell layers, four parvocellular layers at top with small cells and two magnocellular layers at bottom with large cells. Between layers are cone-shaped cells {koniocellular neuron} that code for blue-yellow opponency, the difference between S cones and L+M cones [Calkins, 2000] [Chatterjee and Callaway, 2002] [Dacey, 1996] [Nathans, 1999].
Thin thalamic nuclei {lateral dorsal nucleus} can be in anterior, be for memory and emotion, and send to anterior cingulate gyrus.
Thalamus nucleus {lateral geniculate nucleus}| (LGN) is for object identification [Przybyszewski et al., 2000] [Shepherd, 1998] [Sherman and Guillery, 2001] [Sherman and Koch, 1998].
input
LGN receives from all senses except olfaction, especially from retinal ganglion neurons. It is sensitive to eye position. It has dermatomal segments to represent body sensations.
Thalamus receives much more feedback from cortex than it sends to cortex. Such positive and negative feedback probably applies learned and innate information to bias stimulation, which predicts stimuli [Koch, 1987] [Mumford, 1991] [Mumford, 1994] [Rao and Ballard, 1999].
LGN has circular receptive fields.
output
LGN sends, through optic radiation {geniculostriate pathway, vision}, to visual cortex area V1 in occipital lobe. Geniculostriate and tectopulvinar pathways interact.
LGN sends to somaesthetic cortex.
LGN sends to overlapping, multiple lateral geniculate nucleus cells {relay cell}. Through dendrodendritic connections, LGN affects neurons up to five millimeters away.
Neurons inhibit themselves.
damage
Damage to lateral geniculate causes poor acuity.
anatomy: layers
Lateral geniculate nucleus has six separate cell layers, four parvocellular layers at top with small cells and two magnocellular layers at bottom with large cells. Parvocellular and magnocellular core neurons send to one cortex region.
LGN layers 1, 4, and 6 are for opposite-side eye. Layers 2, 3, and 5 are for same-side eye. Layer 1 and 2 neurons respond to OFF, at any wavelength. Layer 3 and 4 neurons respond to ON or OFF, at wavelength range. Layer 5 and 6 neurons respond to ON, at wavelength range. Layer 3 and 4 neurons have opponent cells for red-green and blue-yellow.
anatomy: magnocellular
Magnocellular cells receive from bipolar cells with bigger dendrite trees and send transient signals to visual-cortex layer 4c-alpha and layer 6. These large cells are for temporal resolution, movement, and flicker. Optic-tract axons from right and left eyes synapse on separate magnocellular neurons, in bands.
anatomy: parvocellular
Parvocellular cells receive from midget cells and send sustained signals to visual-cortex layer 4cbeta. Small cells are for color, spatial resolution, texture, shape, depth perception, and stereopsis [Merigan and Maunsell, 1993] [Schiller and Logothetis, 1990].
anatomy: koniocellular
Between layers are koniocellular neurons {matrix cell} that code for blue-yellow opponency, the difference between S cones and L+M cones [Calkins, 2000] [Chatterjee and Callaway, 2002] [Dacey, 1996] [Nathans, 1999]. Koniocellular cells go to several regions.
anatomy: Y cells
Y cells maintain activity after moving object crosses receptive field, using cortico-thalamic feedback.
color processing
Brain has four opponent processes. Cell can react oppositely to red and green or green and red. Cell can react oppositely to blue and yellow or yellow and blue. Luminance is sum of red and green. Comparisons cross, so the three colors add orthogonally.
Magnocellular cells {magnocellular layer} receive from bipolar cells with bigger dendrite trees and send transient signals to visual-cortex layer 4c-alpha and layer 6. These large cells are for temporal resolution, movement, and flicker. Optic-tract axons from right and left eyes synapse on separate magnocellular neurons, in bands.
Fibers {massa intermedia} link left and right thalamus.
Peanut-sized thalamus nuclei {medial dorsal nucleus} can be for emotions and receive from and send to amygdala and prefrontal cortex, mostly orbitofrontal cortex. Intralaminar nuclei surround it.
Thalamus nuclei {medial geniculate nucleus} can be for sound; receive from cochlea, lateral lemniscus, and inferior colliculus; and send to temporal lobe.
Lateral thalamic nuclei {medial lateral thalamic nucleus} can be for memory.
Thalamic regions {medial lemniscus} can mix input from touch receptors, thermoreceptors, and nociceptors along spinothalamic tract. Descending inhibition enhances contrast between stimulated area and adjacent regions or admits only certain input to higher levels, and so affects attention.
Parvocellular cells receive from bipolar cells with small dendrite trees {midget cell} and send sustained signals to visual-cortex layer 4cbeta. Small cells are for color, spatial resolution, texture, shape, depth perception, and stereopsis [Merigan and Maunsell, 1993] [Schiller and Logothetis, 1990].
Thalamus regions {motor thalamus} can connect to basal ganglia, cerebellum, motor neocortex, vagus nerve, and hypothalamus and is in visceral and autonomic system.
Parvocellular cells {parvocellular layer} receive from midget bipolar cells with small dendrite trees and send sustained signals to visual-cortex layer 4cbeta. Small cells are for color, spatial resolution, texture, shape, depth perception, and stereopsis [Merigan and Maunsell, 1993] [Schiller and Logothetis, 1990].
Thalamus nuclei {pulvinar nucleus} can have inferior, lateral, and medial nuclei that are for attention, are multisensory, and receive from superior colliculus and retinal ganglion cells [Desimone et al., 1990] [Grieve et al., 2000] [Kinomura et al., 1996] [LaBerge and Buchsbaum, 1990] [LaBerge, 2000] [Rafal and Posner, 1987] [Robinson and Cowie, 1997] [Robinson and Petersen, 1992]. Pulvinar nucleus excites posterior parietal and inferior temporal lobes for external stimuli. Nucleus sides {lateral pulvinar nucleus} inhibit cerebral cortex to suppress irrelevant events, increase resolution, minimize receptive fields, and specify attention focus.
Thin cell sheet {reticular nucleus} {nucleus reticularis thalami} (nRt) surrounds thalamus and has only inhibitory GABA neurons. Reticular nucleus receives from most axons to and from neocortex and interacts with its own neurons. It sends output to thalamus, to organize sleep rhythms, such as deep-sleep spindling and delta waves, and select sense channels to cortex.
thalamus nucleus {semilunaris nucleus}.
Thalamus regions {sensory thalamus} can have reverberatory circuit from reticular formation and hypothalamus to cortex. It carries wakefulness impulses. It mediates contact, temperature, and pain consciousness. It has anterior, lateral geniculate, medial-lateral, pulvinar, semilunaris, and ventral centrum medianum nuclei.
Motor nucleus {ventral anterior thalamic nucleus} receives from cerebellum and globus pallidus and sends to corpus striatum.
thalamus nucleus {ventral centrum medianum nucleus}.
Motor nucleus {ventral lateral thalamic nucleus} receives from cerebellum and globus pallidus and sends to cerebral motor cortex.
Thalamic region {ventral medial basal thalamus} receives from parabrachial nucleus and nucleus tractus solitarius and sends to posterior insula.
Thalamic region {ventral medial posterior thalamus} receives from trigeminal nucleus and sends to posterior insula.
Thalamic region {ventral posterior thalamic nuclei} includes sensory ventral posterolateral nucleus and ventral posteromedial nucleus. It receives from medial lemniscus, spinothalamic tract, and trigeminal nerve and sends to postcentral gyrus.
Thalamus nucleus {ventrobasal complex} receives from dorsal column nuclei and sends to primary somatosensory cortex.
Cerebrum has frontal region {frontal lobe}| [Barcelo et al., 2000] [Brickner, 1936] [Churchland, 2002] [Colvin et al., 2001] [Damasio and Anderson, 2003] [Dennett, 1969] [Eliasmith, 2000] [Fuster, 2000] [Nakamura and Mishkin, 1980] [Nakamura and Mishkin, 1986].
purposes
Frontal lobe stores systematic semantic concepts and relationships. It analyzes and stores somatosensory, visual, and auditory information. It anticipates motor and cognitive effects. It is about attention, arousal, anxiety, and mood. It affects spatial, recognition, and short-term memory.
purposes: behavior
Frontal lobe establishes action plans and maintains motivations. It controls movement schedule and sequence. It regulates motor, emotional, sexual, and appetitive behaviors. It controls bipedal posture and habituation. It determines energy level and interests. When preparing for motion, frontal-cortex neurons have high-frequency oscillations.
damage
Frontal-lobe damage can impair voluntary movements and delayed responses. Damage can cause hyperactivity, after one day. Damage can eliminate chronic pain responses. Damage can cause no-emotion states. Damage can prevent solving problems that have multiple answers or that require multiple object views. Damage can cause repeated behavior {perseveration, frontal lobe}, as shown by Wisconsin card-sorting test. Damage can cause impaired associational learning. Damage can reduce introspection and daydreaming. Damage can prevent goals. Damage can cause people not to know that they are deficient.
anatomy
Frontal lobe connects to nucleus accumbens, locus coeruleus, hypothalamus, limbic system, precentral cortex, striatum, and posterior parietal, prestriate, and temporal lobes.
attention
Attention affects frontal lobe [Huerta et al., 1986] [Schall, 1997].
Frontal-cortex midline gyrus {anterior cingulate gyrus} {anterior cingulate cortex} (ACC) is for attention, consciousness, voluntary control, and pain. It measures pain unpleasantness. It has Brodmann areas 24, 25, 32, and 33. Multisensory cells resolve conflicts between signals, such as Stroop effect.
Left-frontal-lobe inferior regions {Broca's area} {Broca area}, above lateral sylvian fissure, in front of motor cortex, control speech muscles that make grammatical language [Di Virgilio and Clarke, 1997].
Broca's area and Wernicke's area connect {arcuate fasciculus}.
Broca's area seems to have existed in Homo habilis.
Frontal-lobe midline region {cingulate gyrus}| surrounds corpus callosum.
Frontal-lobe areas {entorhinal area} {entorhinal cortex} can connect to hippocampus, dentate gyrus, sensory frontal lobe, temporal lobe, cingulate neocortex, and olfactory cortex. Entorhinal cortex receives from olfactory bulb. Entorhinal cortex sends sense input to hippocampus.
damage
Entorhinal cortex loss causes inability to consciously remember facts or events, such as new category members or unique examples. Damage does not affect perceptual-motor skills with no conscious internal representations, such as mastering task over several sessions or retrieving previously acquired factual knowledge.
evolution
Entorhinal cortex developed early in evolution.
Frontal-lobe interior orbital surface posterior part {insula, brain}| {insular cortex} includes amygdala and hippocampus. Posterior insula receives from ventral medial posterior thalamus and ventral medial basal thalamus and sends to anterior insula, which sends to anterior cingulate and ventromedial frontal lobes. Insula controls trophotropic behavior through parasympathetic nervous system. Anterior insula responds to pictures of self. Insula receives from taste neurons. Insula helps recognize consonants.
Left lateral frontal lobe {left lateral frontal lobe} stores word meanings, together with Wernicke's area [Churchland, 2002] [Dennett, 1969] [Eliasmith, 2000]. Damage blocks understanding of verb classes but not noun classes.
Damage to fusiform and lingual gyri {lingual gyri} causes no color perception.
Frontal-lobe neuron system {mirror-neuron system} {mirror neuron}, in rostral ventral premotor area F5, allows perception, understanding, and action imitation. Neurons are active when people perform actions and when other people perform same actions. Brain connects voluntary-muscle commands, proprioception, visual perception, and sounds.
theories
Perhaps, action recognition recreates motor-brain-area motor action {direct-matching hypothesis}. Perhaps, perceptual brain areas analyze perceptions by context, body parts used, and motions caused {visual hypothesis} [Ramachandran, 2004] [Rizzolatti et al., 1996].
Frontal-lobe regions {orbitofrontal cortex} {Brodmann area 11} can be above eye orbit bones, be for smell and affective values, and process learned stimulus-reward associations. It develops before prefrontal cortex.
Brain regions near eye {orbito-frontal lobe} can be for planning, priorities, unexpected, and attention.
A frontal-lobe region {premotor frontal lobe}, Broadmann area 6, between medial motor cortex and dorsomedial prefrontal cortex, stops movements, blocks repetition, coordinates muscles, and is for rehearsal before action or imagination.
Frontal-lobe rostral regions {rostral frontal lobe} can connect to thalamus, hypothalamus, and septum. Rostral frontal lobe is for inherited and acquired social behavior. Large rostral frontal-lobe lesions cause little attention to others' feelings and behavior, failure to greet friend or newly introduced stranger appropriately, emotionless conversation, and failure to say good-bye properly.
Prefrontal regions {supplementary motor area} (SMA), between medial motor cortex and dorsomedial prefrontal cortex, can receive from higher sense regions. SMA applies memories, goals, feelings, and will. It sends to premotor regions, which coordinate and integrate signals sent to motor cortex, and to midline, where brain sequences actions to fit plan {motor plan}. It has readiness potential and lateralized readiness potential.
In insula are hippocampus major {horn of Ammon} and hippocampus minor {hippocampus}| [Freund and Buzsáki, 1996] [Parra et al., 1998].
functions
Hippocampus is for long-term and short-term memory. It is necessary to store new memories, but conscious associative fact and event memory also requires other brain regions. Hippocampus is for motivation, reward, rehearsal, and space. It controls ergotropic behavior through sympathetic nervous system. It detects movement direction, head attitude with respect to body, and movement sequence. Neurons can find relations among facts and experiences. Neurons can find fact and experience conjunctions, while neocortex builds learning structures.
damage
Hippocampus damage blocks habituation to repeated stimulation. Hippocampal formation and parahippocampal cortex loss causes inability to consciously remember facts or events, such as new category members or unique examples. Damage does not affect perceptual-motor skills with no conscious internal representations, such as mastering task over several sessions or retrieving previously acquired factual knowledge. Hippocampus damage does not affect perception, consciousness, habits, skills, language, classical conditioning, instrumental conditioning, or motor control.
damage: Alzheimer's
In Alzheimer's disease, basal-forebrain cholinergic-neuron degeneration causes low hippocampal choline acetyltransferase activity.
input
Parahippocampal gyrus and hippocampus have multisensory cells.
output
Hippocampus sends through septum and nucleus accumbens to hypothalamus. It sends to cholinergic neurons at forebrain base, nucleus basalis magnocellularis, medial septal nucleus, and nucleus of diagonal band of Broca. It connects to medial temporal lobe.
process: memory
Brain stores memory only if cerebral neocortex sends information to three different areas close to hippocampus and then into hippocampus itself. Hippocampus then passes message back through medial temporal lobe to originating site in cerebral neocortex.
process: place
Spatial information travels from thalamus to neocortex to hippocampus. Hippocampus has non-topographic cognitive space map, stored in pyramidal place cells. Place-cell fields are stable and form in minutes [Brown et al., 1998]. Place cells increase firing when body is at that location [Ekstrom et al., 2003] [Frank et al., 2000] [Nadel and Eichenbaum, 1999] [O'Keefe and Nadel, 1978] [Rolls, 1999] [Scalaidhe et al., 1997] [Wilson and McNaughton, 1993] [Zhang et al., 1998]. Place cells also recognize textures, objects, and contexts. For example, they fire only when animal sees face (face cell), hairbrush, or hand.
waves
Hippocampus has 4-Hz to 10-Hz theta rhythm during active movement and alert immobility, synchronized between hemispheres in 8-mm region along hippocampus longitudinal axis. Other behaviors have local and bilaterally synchronous 40-Hz rhythm. A 200-Hz wave associates with alert immobility. Awake brain has synchrony, which increases with attention and preparation for motor acts. When neocortex desynchronizes with low-voltage rapid potentials, hippocampus synchronizes with theta waves. When neocortex synchronizes, hippocampus desynchronizes.
Frontal lobe has hippocampus major, hippocampus minor, and subiculum {hippocampal formation}.
Spatial information travels from thalamus to neocortex to hippocampus. Hippocampus has non-topographic cognitive space map, stored in pyramidal place cells. Some hippocampus neurons {place cell, hippocampus} increase firing when body is at that location [Ekstrom et al., 2003] [Frank et al., 2000] [Nadel and Eichenbaum, 1999] [O'Keefe and Nadel, 1978] [Rolls, 1999] [Scalaidhe et al., 1997] [Wilson and McNaughton, 1993] [Zhang et al., 1998]. Place-cell fields are stable and form in minutes [Brown et al., 1998]. Place cells also recognize textures, objects, and contexts. For example, they fire only when animal sees face (face cell), hairbrush, or hand.
Primate hippocampus has some neurons {spatial view cell} that fire only when viewing or recalling a location (with 30 degrees), no matter what head orientation or body location.
A brain region {limbic system}| {threshold system} {limbic lobe} on frontal-lobe interiors surrounds brainstem. In mammals, limbic system includes amygdala, caudate, cingulate gyrus, entorhinal cortex, fornix, hippocampus, hypothalamus, olfactory cortex, pyriform cortex, preoptic, putamen, septum, and thalamus. It receives from hypothalamus and basal ganglia. It sends to sense and motor cerebral cortex. It connects to sympathetic nervous system for activity and parasympathetic nervous system for relaxation.
Limbic system organizes essential drives, controls visceral processes, and involves emotions, fear, anger, flight, defense, and instincts. It does not integrate emotions.
evolution
Limbic system developed in primitive fish and is the most-ancient cerebral-hemisphere part. Limbic system is more important in mammals that rely on smell more than vision and less important in aquatic mammals and primates.
damage
Damage reduces cerebrum activity, and people enter dreamy state.
Body systems {mesolimbic system} can make cholecystokinin (CCK) peptide and dopamine (DA) catecholamine and send to other limbic system neurons in nucleus accumbens, lateral hypothalamus, ventral tegmentum, olfactory tubercle, and amygdala central nucleus. Schizophrenia causes mesolimbic-system hyperactivity.
Cerebrum rear {occipital lobe}| is for vision, perceptual judgment, memory, and association.
input
Occipital lobe receives from lateral geniculate nucleus, mostly onto layer 4 [Allman, 1998] [Allman and Kaas, 1971] [Zeki, 1974] [Zeki, 1993].
Layer 4 keeps input from two eyes separate. Alternating ocular-dominance-column bands, 0.5 millimeters wide, are for input from same ipsilateral side or opposite contralateral side.
Cortical layers above and below layer 4 have neurons that receive from both eyes. Binocular neurons differ slightly in eye connection alignment, allowing distance judgments.
Occipital lobe also receives from lower brain centers.
damage
Occipital lobe damage causes blindness. Cortical area V1, V2, and V3 damage affects perception and pattern recognition, leaving only ability to perceive intensity. Left-occipital lesion and corpus-callosum posterior-splenium lesion cause alexia without agraphia.
anatomy
Simple cells have well-defined excitatory and inhibitory regions in receptive fields [DeValois and DeValois, 1988] [Hubel and Wiesel, 1959] [Hubel and Wiesel, 1962] [Hubel, 1988] [Livingstone, 1998] [Spillman and Werner, 1990] [Wandell, 1995] [Wilson et al., 1990].
Complex cells do not have well-defined excitatory and inhibitory regions [Allman et al., 1985] [Gallant et al., 1997] [Lamme and Spekreijse, 2000] [Shapley and Ringach, 2000].
Complex-neuron receptive fields are larger than simple-neuron fields and have up to 100 degrees of visual angle.
processing
Some visual-cortex neurons distinguish between familiar and unfamiliar objects. Some neurons recognize faces. Some neurons respond only to face, hairbrush, or hand. Some neurons respond to face only if eyes point in direction. Some neurons store object locations. Some neurons predict eye-movement direction.
Visual-cortex layers 2 and 3 neuron groups {blob} and layers 4B, 5, and 6, separated by 0.4 to 1.0 millimeters, detect color and brightness, but not orientation, at space point [Conway et al., 2002] [Lennie, 2000] [Livingstone and Hubel, 1984] [Livingstone and Hubel, 1988] [Michael, 1978] [Michael, 1981]. Blob center-surround cells are for white-black and black-white, red-green and green-red opponent, and red-green and blue-yellow double opponent.
Visual-cortex layer-4 neurons {calcarine cortex} receive input from lateral geniculate nucleus and other brain sites. Cortical layers 3, 2, 1, and 6 repeat neural array in visual-cortex layer 4.
input
One quarter of neurons use input from right eye. One quarter use input from left eye. One quarter use input from both eyes with right eye dominant. One quarter use input from both eyes with left eye dominant.
Half have receptive fields with excitatory center. Half have inhibitory center.
Half are for shape and color detection. Half are for texture and motion detection.
100 billion neurons converge on 100 million output neurons in visual-cortex layer 5 and lower-4.
point processing
For space plane-surface points, brain has 30 neurons to detect features, such as line-segment orientation. The 30 neurons are in a circle and cover ranges, such as orientations.
receptive fields
Brain has neurons with different-size receptive fields, to detect different-size features, from point size, 0.1 millimeters, to whole-visual-field size, 1000 millimeters.
density
Neurons are denser at brain points corresponding to retina center and are less dense for retina edge.
maps
Visual cortex has maps for shape, depth, color, motion, and texture that interconnect. For features, visual cortex has repeated maps to represent different times in sequence.
number
Space plane-surface points have 4*2*2*30*5 = 2400 visual-cortex neurons. If point number is 1,000,000, then black-and-white representation requires 2,400,000,000 neurons. Color requires 7,200,000,000 neurons. If times differ by 200 milliseconds over three-second intervals, neuron number for visual information totals 100,000,000,000.
Occipital and temporal lobe region {circumstriate cortex} codes patterns and motion relations.
Visual-cortex superficial layers have color-sensitive neuron clusters {color blob}, at macrocolumnar intervals.
Region near ventral temporal lobe {dorsolateral visual area} {area DL} detects visual stimuli length, width, and stimulus position. It detects light-on-dark, dark-on-light, and contrast. It has large excitatory receptive fields, larger than optimum stimulus. It sends to inferotemporal cortex.
Occipital regions {ectosylvian visual area} can send to superior colliculi.
Around striate cortex are areas V2, V3, and V4 {extrastriate cortex, brain} [Bullier et al., 1994] [Hadjikhani et al., 1998].
Visual-cortex neurons respond to orientation, size, contrast, motion direction, motion speed, color, length, and depth {feature detector} in visual space. Neurons are switches that route messages, and states contain messages. Nerve signals from other neurons, muscles, and glands affect feature detectors. Feature detection is generalized associative learning, which can cause actions.
Visual association area 18, area 19, and posterior area 37 {inferior occipital lobe} bilateral damage prevents unique object recognition and feature retrieval. Area 18 and 19 bilateral damage prevents color perception.
Visual-cortex left striate region {intermediate medial hyperstriatum ventrale} (IMHV) is for filial imprinting.
Occipital regions {left posterior occipital lobe} can combine individual letters into one chunk {visual word form} and discriminate between words and non-words 200 milliseconds after input.
Words and pseudo-words, but not consonant strings, excite occipital region {left ventral occipital lobe}.
Occipital-lobe and parietal-lobe regions {occipito-parietal lobe} can be for thinking about two seen things simultaneously.
Occipital-lobe region {parastriate cortex} damage can cause blindness or word blindness.
Occipital-lobe area V4 and V4A region {posterior lunate sulcus} analyzes color and color constancy.
Occipital-lobe regions {posterior occipital lobe} can be for concrete low-complexity knowledge.
Occipital regions {posterior prestriate area} can attend to color, motion, or form.
Occipital regions {V1 brain area} {area V1} {primary visual cortex} {Brodmann area 17} {striate cortex} {striate occipital cortex} {area OC} can be for primary vision perception [Brewer et al., 2002] [Dantzker and Callaway, 2000] [Preuss, 2000] [Preuss et al., 1999] [Sawatari and Callaway, 2000] [Vanduffel et al., 2002].
input
Area V1 receives from lateral geniculate nucleus.
output
Area V1 sends feedback {shifter circuit, vision} to lateral-geniculate-nucleus left-and-right-eye layers, which excite or inhibit cortical-area activity [Ahmed et al., 1994] [Budd, 1998] [Douglas et al., 1995] [Felleman and Van Essen, 1991] [Fries, 1990] [LeVay and Gilbert, 1976] [Saint-Cyr et al., 1990] [Sherk, 1986] [White, 1989].
Area V1 sends orientation information to area V2 and then to area V5.
Area V1 sends object recognition and color information to area V2, then to area V4, and then to inferotemporal cortex.
Area V1 sends object location and movement information to area V2, then to area V5, and then to inferior parietal cortex.
Area V1, area V2, area V3, and mediotemporal cortex layer-5 pyramidal cells send to superior colliculus superficial layers and to pons nuclei.
Layer-6 pyramidal-cell axon collaterals synapse on aspinous inhibitory interneurons [Callaway and Wiser, 1996].
anatomy
Striate occipital cortex has visual-field map accurate to one millimeter. Map has ocular dominance columns for both eyes. Map has orientation columns, in which preferred orientation shifts through complete cycle in 0.5 to 1 millimeter. Thousands of orientation and ocular dominance columns cross each other at right angles. Neurons that prefer particular spatial frequency, color, or size also cluster [Engel et al., 1997] [Gur and Snodderly, 1997].
Around striate cortex are areas V2, V3, and V4 {extrastriate cortex, vision} [Bullier et al., 1994] [Hadjikhani et al., 1998].
processing: edge
Most area-V1 neurons respond best to one light or dark edge-or-thin-bar orientation. Edge or bar can be stationary, moving, or flashing.
processing: line
Concentric circles on retina are parallel lines in V1.
processing: letters
Area V1 is active while visualizing letters, even with eyes closed. V1 anterior part, for parafoveal input, is more active for large size letters. V1 posterior part, for foveal input, is more active for small size letters.
processing: binocular
Striate cortex combines signals from both eyes, as do most cells in visual cortex.
processing: attention
Attention affects area V1 [Brefczynski and DeYoe, 1999] [Fries et al., 2001] [Gandhi et al., 1999] [Ito and Gilbert, 1999] [Ito et al., 1995] [Kastner and Ungerleider, 2000] [Motter, 1993] [Niebur and Koch, 1994] [Niebur et al., 1993] [Niebur et al., 2002] [O'Connor et al., 2002] [Roelfsema et al., 1998] [Somers et al., 1999] [Watanabe et al., 1998].
factors: saccade
Spontaneous area-V1-neuron activity decreases when eye moves {saccadic suppression, V1} [Bridgeman et al., 1975] [Burr et al., 1994] [Castet and Masson, 2000] [Haarmeier et al., 1997] [Ilg and Thier, 1996] [McConkie and Currie, 1996].
Saccade target object excites some V1 cells and more V2 cells.
evolution
All mammals have areas V1 and V2, which combine visual, auditory, and tactile sense data. Perhaps, more trunk-and-neck flexibility and limb development allowed those areas.
Occipital regions {V2 brain area} {area V2} can be for stereoscopic vision [Engel et al., 1997] [Heydt et al., 2000] [Levitt et al., 1994] [Livingstone and Hubel, 1981] [Livingstone and Hubel, 1987] [Merigan et al., 1993] [Peterhans, 1997] [Roe and Ts'o, 1997] [Thomas et al., 2002] [Tootell et al., 1998] [Wong-Riley, 1994].
Almost all area V2 neurons receive input from both eyes. Color, location, and shape have alternating area-V2 bands. Nearness and farness cells detect distance. Area V2 neurons have bigger receptive fields than neurons in area V1. V2 neurons can respond to illusory edges, hidden and seen shapes, or figure-ground differences.
output
Almost as many neurons send to area V1 from area V2 as send from V1 to V2.
Occipital regions {V3 brain area} {area V3} can be for depth of vision [Burkhalter and Van Essen, 1986] [Lyon and Kass, 2002] [Newsome and Pare, 1988] [Newsome et al., 1986] [Newsome et al., 1989] [Tootell et al., 1997] [Zeki, 2003]. Nearness and farness cells detect distance. Some cortical-area-V3A neurons respond to gaze angle.
Ventral-system occipital regions {V4 brain area} {area V4} are for color perception and have topographic maps. Lunate sulcus posterior part and superior temporal sulcus anterior part are for color and color constancy. Area V4 responds to all wavelengths and line orientations but does not respond to movement. Some neurons are sensitive to spots or rectangles. Nearness and farness cells detect distance. Area-V4 visual neurons also respond to somatosensory stimuli [Burkhalter and Van Essen, 1986] [Newsome and Pare, 1988] [Newsome et al., 1986] [Newsome et al., 1989] [Tootell et al., 1997] [Wachtler et al., 2003] [Zeki, 1973] [Zeki, 1983] [Zeki, 1993]. Perhaps, cells are in color columns.
attention
Attention affects area V4 [DeWeerd et al., 1999] [Ghose and Maunsell, 2002] [McAdams and Maunsell, 1999] [Treue and Martinez-Trujillo, 1999].
color
Some cells are opponent, and some double-opponent. Some cells are for specific colors, orientations, and shapes. Some cells are for any color differences [DeValois and DeValois, 1975].
Ventromedial occipital-lobe regions {V6 occipital brain area} {area V6, occipital lobe} can be for color.
Ventral and medial occipital lobe region {ventromedial occipital lobe} damage causes color vision loss. Practice can reduce damaged region.
Ventral and posterior occipital regions {ventroposterior occipital lobe} {area VP} can be for color.
In occipital lobe, maps {visual buffer}, with retina input, can segregate figure from ground during perception and store images.
Vision cortex {visual cortex}| measures surface area and spatial frequency. It has same number of stellate neurons as pyramidal cells. Cerebral cortex has more than 30 visual or mixed areas, and half have maps with input from retina. Primates have more than 21 visual areas: V1, V2, MT, and M. V1 has calcarine fissure.
input
It receives excitatory axons one-third from same-side lateral geniculate nucleus and reticular nuclei. It receives inhibitory axons two-thirds from same-side locus coeruleus. It does not receive many axons from association areas or from other brain half.
output
It sends to superior colliculus, lateral geniculate nucleus, and area-17 and area-19 superficial pyramidal neurons, up to three millimeters away.
A brain region {parietal lobe}| between frontal and occipital lobes and above temporal lobe is for movement, orientation, calculation, and recognition. It controls symbol use, spatial orientation, maps, space in general, body-side consciousness, numerical and logical relations, and sense associations. It understands speech parts, passive voice, and possessive case, in different subregions. It is for language, learning, and memory. It, mostly inferior parietal, participates in memory retrieval.
Attention affects parietal lobe [Bisley and Goldberg, 2003] [Colby and Goldberg, 1999] [Gottlieb et al., 1998].
damage
Parietal lobe damage disrupts memory, spatial cognition, and attention. Parietal lobe damage causes anomalous body experiences. Non-dominant, usually right, posterior parietal lobe damage can cause hemi-neglect and anosagnosia.
Parietal lobe regions {angular gyrus}| can be for reading and writing, detect number concepts such as cardinality and ordinality, and connect speech-behavior auditory information to visual information. Perhaps, left side is multisensory, and right is spatial [Ramachandran, 2004]. Angular gyrus expanded greatly from mammals to humans.
Parietal-lobe regions {primary auditory cortex} {area A1} {A1 area} can be adjacent to Wernicke's area and receive from medial geniculate nucleus, which receives from inferior colliculus, which receives from nucleus {lateral lemniscus nucleus}, superior olive, and cochlear nuclei. Lateral lemniscus nucleus receives from superior olive and cochlear nuclei. Superior olive receives from dorsal, posteroventral, and anteroventral cochlear nuclei and both ears. Cochlear nuclei receive from cochlea {spiral ganglion} auditory neurons.
processing
Y cells maintain activity after moving object crosses receptive field, using cortico-thalamic feedback.
Parietal regions {auditory cortex}| can be for hearing, sound, octaves, and tone patterns. It has frequency-sensing neuron field perpendicular to intensity-sensing neuron field.
processing
Specific brain places recognize sounds in word, speech, or sentence. Special places are for object names, word productions, writing, remembering words, and speaking spontaneously.
No matter the musical scale, people prefer octave tuned slightly higher than exact 2:1 frequency ratio.
damage
Primary hearing area destruction causes only high-tone loss. Bats can hear even with damaged primary auditory areas.
Auditory-cortex regions {corticofugal network} can learn sound patterns and send dopamine feedback to itself and higher regions.
Parietal-lobe back regions {dorsal parietal lobe} can be for well-being feeling.
Cells {grasping cell} can respond to grasping.
Inferior parietal lobe regions {inferior parietal lobe} (IPL) {caudal inferior parietal lobe} can have two main parts, LIP and 7a. Both LIP and area 7a receive input from thalamus medial pulvinar nucleus. Area LIP sends to superior colliculus and frontal eye fields to execute saccadic eye movements. Area 7a sends to polymodal cortex, limbic system, and prestriate cortex, to detect retinal locations and eye and head positions. Right or left Brodmann-area-7 damage causes hemi-neglect.
Speech area damage {left anterior parietal lobe} can harm syntax, sequential organized speech, and skilled movements but not affect phoneme, word, logic, or grammar production or understanding.
Left inferior parietal region {left inferior parietal} damage affects color-perception achromatopsia in fusiform gyrus, motion-perception akinetopsia in mediotemporal region, face perception in prosopagnosia, and feelings that there are imposters in Capgras syndrome [Nordby, 1990] [Perrett et al., 1992] [Scalaidhe et al., 1997] [Tranel and Damasio, 1985].
Association area {left inferoparietal} damage can cause various language problems.
Association area {left parieto-occipital} damage can cause various language problems.
Speech area damage {left posterior parietal lobe} can interfere with language acquisition and harm paradigmatically-organized speech production and understanding, but not affect syntax and organized speech.
Posterior area V4 and V4A regions {lunate sulcus} can analyze color and color constancy.
Human parietal-lobe regions {motor cortex}| {area M1} {Brodmann area 4} {precentral gyrus} {pre-central gyrus} {motor strip} can have two or three million motor neurons, control purpose, initiate voluntary movements, activate habits, cause automatic movements, and specify muscle positions needed at movement completion. Pre-central gyrus contains most corticospinal motor tract neurons.
output
Motor-cortex pyramidal neurons send to extrapyramidal-motor-system alpha and gamma motor neurons, to coordinate and initiate fast and precise movements. Motor neurons excite spinal cord neurons, which excite special muscle fibers in muscle spindles. Primary motor cortex connects to basal ganglia, thalamus, and other cerebral cortex [Bullock et al., 1977].
processing
Muscles move to reach specified muscle positions, as registered by muscle sensors. Motor cortex programs movements by controlling lower-level reflexes. Once started, motor program cannot stop, only change. Motor cortex neurons align by movement direction. Neurons signal particular limb-movement direction. Actual movement is sum of vectors. Primary motor cortex M1 activity shifts with intended-arm-movement coordinates [Amirikian and Georgopoulos, 2003] [Bullock, 2003] [Dean and Cruse, 2003] [Evarts, 1968] [Miall, 2003].
In isotonic movement, motor cortex and red nucleus neurons give intense burst, at frequency corresponding to movement velocity and duration corresponding to movement duration. In isotonic movement, Purkinje cells give bursts or pauses, to inhibit positive feedback to antagonists or allow positive feedback to agonists. In isometric movement, motor cortex and red nucleus neurons give intense burst, at frequency corresponding to force and duration corresponding to force rate. Motor cortex and red nucleus neurons can also have tonic output.
Sense information selects motor-program parameters to initiate program, to define movement endpoint through proprioception, and to guide subsequent adaptive process that mediates motor learning. Sense feedback shapes motor map, and vice versa.
Y cells maintain activity after moving object crosses receptive field, using cortico-thalamic feedback.
Muscle activity initiation always begins unconsciously in cerebrum. Conscious control can affect final motor nerve signals.
damage
Damage to motor cortex does not change learned mammal behavior patterns.
voluntary movement
Mammals have voluntary behavior and move bodies and appendages to specific space points {voluntary movement}.
voluntary movement
The two million motor neurons of human parietal-lobe motor-cortex area M1 initiate voluntary movements and specify muscle positions needed after movements. Muscles move to reach specific muscle positions, as registered by muscle sensors. Motor-cortex pyramidal neurons send to spinal-cord lateral corticospinal tract, which controls voluntary muscles by controlling reflexes.
vectors
Motor-cortex neurons contract specific muscle fibers, which move in relative direction from zero length change up to maximum length change. Fiber movements have magnitude and direction and so are vectors.
vector sums
Individual cortical cells have few connections to nearby neurons, so individual-neuron activation cannot provide enough signal strength to start or maintain movements {motor act}. Motor acts require multiple neuron pathways to achieve precise movement timing. Motor acts generate large precisely coordinated temporal-signal sequences to activate muscles. In contralateral superior colliculus, average neuron vector directs eye movement, or eye and head movement, to target object, using body-centered coordinates.
Neurons for attention to target control motor neurons. Brains control movements using few independent parameters. Motor acts require coordinated temporal motor-neuron activation and inhibition. To move limbs or body parts in specific directions, motor-cortex neurons contribute fiber movement. Total limb or body-part movement is sum of vectors and moves limb or body part from starting position to final position, using body-centered coordinates. Motor cortex accounts for starting position, finds vector sum, and moves to intended final position. Proprioceptive sense information defines starting and ending positions [Amirikian and Georgopoulos, 2003] [Bullock, 2003] [Dean and Cruse, 2003] [Miall, 2003].
input
Input from attention, planning, and drive neurons goes to all motor neurons.
movement-control parameters
Movement control uses several independent parameters. For isotonic movements with constant force, motor-cortex neurons fire for duration corresponding to movement duration, at rate corresponding to movement velocity. For isometric movements with no motion, motor-cortex neurons fire for duration corresponding to force duration, at rate corresponding to force.
In primates, parietal regions {area MT} {MT area} can analyze small object and large background motions and orientation. Adjacent neurons detect slightly different orientations in one direction and opposite orientations in perpendicular direction. MT also participates in recognition memory.
Parietal-lobe anterior-edge regions {post-central gyrus} can be tactile and kinesthetic sense areas. Its SI topographic map has Penfield homunculus.
Parietal lobe has posterior region {posterior parietal lobe} (PP) [Andersen, 1995] [Batista and Andersen, 2001] [Bisley and Goldberg, 2003] [Bruce et al., 1986] [Colby and Goldberg, 1999] [Glickstein, 2000] [Gross and Graziano, 1995] [Snyder et al., 2000].
input
Posterior parietal lobe receives from visual, auditory, and proprioceptive cortex.
output
Posterior parietal lobe sends to inferior-temporal-lobe superior temporal sulcus superior boundary, spinal cord, brainstem, prefrontal lobe, and frontal lobe.
functions
Posterior parietal lobe detects sense location, size, orientation, and motion direction. It represents attended object locations. It is for attention, shape transformations, category and spatial coordinate interactions, spatiotopic mapping, and spatial relations. In humans, it is about spatial cognition, in right hemisphere, and language understanding, in left hemisphere. It registers movement consequences, such as current eye position. Eye position multiplies receptive-field event [Zipser and Andersen, 1988]. It plans and initiates limb movements in primates. Map in cortical area 6 computes locations in nearby space, using body-based coordinates, and can guide orienting responses, like tectofugal pathway. Cortical area 7b has map of nearby space for motor control. Neurons respond to both receptive field changes and eye or head position [Andersen et al., 1985] [Andersen et al., 1997] [Pouget and Sejnowski, 1997] [Salinas and Abbott, 1995].
Parietal regions {suprasylvian visual area} can send to superior colliculi.
In primates, left-inferior parietal-lobe association regions {Wernicke's area} {Wernicke area} can be in left-superior temporal lobe below lateral fissure, next to primary auditory cortex, at vision, audition, and somaesthetic cortical junction. Wernicke's area has no connections to limbic system. Broca's area and Wernicke's area connect through arcuate fasciculus.
damage
Wernicke's area damage causes alexia, agnosia, tactile aphasia, and word deafness but does not affect writing or hearing. Disconnecting Wernicke's area from motor centers causes apraxia. Wernicke's aphasia causes bad semantics, paraphasia, imprecise words, circumlocutions, and neologisms, but speech is fluent, rapid, articulated, and grammatical.
Cerebral neocortex {prefrontal lobe}| {prefrontal cortex} can be behind frontal lobe [Carmichael and Price, 1994] [Fuster, 1997] [Goldberg, 2001] [Grafman et al., 1995] [Miller and Cohen, 2001] [Passingham, 1993] [Preuss, 2000].
functions
Prefrontal lobe activates brain, is for attention, is for emotion cognition, controls respiration and autonomic system, causes initiative and persistence, foresees consequences, and forms intentions.
Lateral prefrontal cortex is for temporary storage in working memory. Anterior cingulate in medial prefrontal cortex is for executive functions and coordinates information about self. Ventral prefrontal and orbital cortex is for emotions and participates in memory retrieval.
input
Prefrontal lobe has many dendrite D1 and D5 dopamine receptors. Prefrontal cortex receives from mediodorsal thalamic nucleus.
output
Of all neocortex, only prefrontal sends directly to hypothalamus. It also sends to basal ganglia striatum and globus pallidus.
damage
Prefrontal lobe damage causes selfishness, bad manners, inability to concentrate, failure to plan, inability to think abstractly, and indifference.
evolution
Lateral prefrontal cortex is only in primates. Ventral prefrontal lobe, orbital cortex, and medial-prefrontal-cortex anterior cingulate are only in mammals.
Brain top and side regions {dorsolateral prefrontal cortex} can be for spatial coordinates and categorization. It looks up information in associative memory to access stored information for working memory. It uses model similar to cerebellar model to control muscle movement and learn new physical skills.
attention
Dorsolateral prefrontal cortex, cingulate nucleus, frontal eye fields in area 8, posterior parietal lobe in area 7a, pulvinar nucleus, and superior colliculus shift attention.
rule
Ventrolateral prefrontal cortex, Brodmann areas 44, 45, and 47, and dorsolateral prefrontal cortex, Brodmann areas 9 and 46, process conditionals. They develop after orbitofrontal cortex and before rostrolateral prefrontal cortex. Orbitofrontal cortex processes rules.
task
Rostrolateral prefrontal cortex, Brodmann area 10, can process task sets. It develops after dorsolateral and ventrolateral prefrontal cortex.
Prefrontal regions {prefrontal medial subgenual region} can be for meaning and mood.
Prefrontal regions {prefrontal ventromedial cortex} can be for sense integration.
Side brain regions {temporal lobe}| can receive information about features, orientations, balance, and sound and have speech-recognition systems. Inside area is for short-term memory, affective memory, and association.
input
Middle-temporal-lobe V5 area detects pattern directions and speed gradients. Medial superior temporal lobe dorsal area detects heading. V2 and V4 areas detect non-luminance-contour orientations. V4 area detects curved boundary fragments. Inferotemporal lobe (IT) detects shape parts. IT and CIP detect curvature and orientation in depth from disparity.
output
Temporal lobe sends to limbic system.
damage
Temporal-lobe lesions can cause the feeling that one has previously witnessed a new situation. Temporal lobe removal decreases pattern discrimination, color vision, fear reactions, learning sets, and retention. Temporal lobe electrical stimulation causes fear, sadness, or loneliness. Removing both temporal lobes makes monkeys fail to recognize objects, be hypersexual, exhibit compulsive oral behavior, not be afraid of things that used to cause fear, and be less aggressive {Klüver-Bucy syndrome, monkey} [Klüver, 1933].
Anterior and inferior temporal-lobe region {anterior inferotemporal area} {area TE} responds to color, shape, and texture over large areas. It detects curves, corners, blobs, and other features. It receives from posterior inferotemporal and medial temporal and sends to prefrontal, medial temporal, and striatum. It has no topographic maps. Eye or head movements do not affect it [Wang et al., 1996].
Temporal-lobe {anterior temporal lobe} damage can block fact retrieval and affect speech.
Extrastriatal gyrus {fusiform gyrus}| in middle and inferior ventral temporal lobe and ventral occipital lobe stores categories, shapes, and patterns. Fusiform gyrus contains area V4, which detects color. A fusiform-gyrus region {fusiform face area} can detect faces [Cowey and Heywood, 1997] [Damasio et al., 1980] [Gallant et al., 2000] [Hadjikhani et al., 1998] [Haxby et al., 2000] [Kanwisher et al., 1997] [Meadows, 1974] [Ramachandran, 2004] [Sakai et al., 1995] [Tong et al., 2000] [Tootell and Hadjikhani, 2001] [Vuilleumier et al., 2001] [Wade et al., 2002] [Zeki, 1990] [Zeki et al., 1991] [Zeki et al., 1998].
damage
Fusiform and lingual gyri damage causes no color perception.
Brain has inferior temporal cortex region {inferotemporal cortex}| (IT) [DiCarlo and Maunsell, 2000] [Gross, 1998] [Gross, 2002] [Logothetis and Sheinberg, 1996] [Tamura and Tanaka, 2001] [Tanaka, 1996] [Tanaka, 1997] [Tanaka, 2003] [Tsunoda et al., 2001] [Wang et al., 1996] [Young and Yamane, 1992].
functions
IT affects visual recognition by visual cortex. IT analyzes complex visual stimuli and discriminates visual forms. IT is for attention and visual memory. IT selects object to view.
IT responds best to new stimuli. If new visual feature matches the original, brain suppresses half of inferotemporal neurons activated by visual feature. One-third of inferotemporal neurons decrease response to familiar or repeated stimuli.
Some inferotemporal neurons recognize individual faces at different views, face prototypes, or poses, ignoring brightness.
Some inferotemporal neurons respond to stimulus actively held in memory and receive back projections from prefrontal cortex [Miyashita et al., 1996] [Naya et al., 2001] [Sheinberg and Logothetis, 2001].
input
IT receives from dorsolateral visual area.
output
IT sends to object recognition centers and attention and orientation systems.
damage
Inferior temporal lobe damage causes inability to categorize or discriminate.
Area 20 and 21 {left anterior inferotemporal} damage impairs object naming, though people can describe objects, have good grammar and phonetics, and name actions and relationships [Wang et al., 1996].
Temporal pole {area 38} {left anterior temporal lobe} damage impairs object naming, though people can describe objects, have good grammar and phonetics, and name actions and relationships.
Verbal-acoustic areas {left temporal lobe} can be for phoneme and word understanding.
Temporal regions {middle temporal lobe} {medial temporal lobe} (MT) {mediotemporal cortex} {V5 brain area} {area V5} can encode motion perception and respond to movement and movement direction but not to wavelength. MT can detect movement direction, from visual texture [Albright, 1993] [Allman and Kaas, 1971] [Andersen, 1997] [Britten et al., 1992] [Britten et al., 1996] [Cook and Maunsell, 2002] [Ditterich et al., 2003] [Goebel et al., 1998] [Goldstein and Gelb, 1918] [Heeger et al., 1999] [Hess et al., 1989] [Heywood and Zihl, 1999] [Huk et al., 2001] [Humphreys, 1999] [Mather et al., 1998] [Parker and Newsome, 1998] [Salzman and Newsome, 1994] [Salzman et al., 1992] [Schall, 2001] [Shadlen et al., 1996] [Tootell and Taylor, 1995] [Tootell et al., 1995] [Tolias et al., 2001] [Williams et al., 2003] [Zeki, 1974] [Zeki, 1991] [Zihl et al., 1983].
MT neurons can code for depth [Bradley et al., 1998] [Cumming and DeAngelis, 2001] [DeAngelis et al., 1998] [DeAngelis and Newsome, 1999] [Grunewald et al., 2002] [Maunsell and Van Essen, 1983].
memory
Medial temporal lobe stores long-term declarative explicit memories. MT also participates in recognition memory.
attention
Attention affects medial temporal lobe [McAdams and Maunsell, 2000] [Saenz et al., 2002] [Treue and Martinez-Trujillo, 1999].
anatomy
MT includes amygdala, entorhinal cortex, hippocampus, parahippocampal gyrus, perirhinal cortex, and Brodmann areas 28, 35, 36, and 37.
input
MT receives from V1 and superior colliculus. Parahippocampal and perirhinal cortex both receive from somatic, auditory, and visual sensory cortex. Entorhinal cortex receives from parahippocampal and perirhinal cortex. Hippocampus DG region receives most from entorhinal cortex and some from parahippocampal and perirhinal cortex, not from neocortex. Hippocampus CA3 receives from DG. Hippocampus CA1 receives from CA3. Subiculum, in hippocampal formation, receives from CA1.
output
MT sends to superior colliculus, posterior parietal lobe, lateral intraparietal lobe, ventral intraparietal lobe, medial superior temporal lobe, and frontal lobe. MT connects through pons nuclei to cerebellum to control body and eye movements. Subiculum sends to rhinal cortex, which sends to sensory cortex.
damage
MT damage over wide area impairs factual knowledge retrieval but not information about categories or object features. Damage impairs smell but nothing else. Damage does not affect attention. Damage also affects emotions. Damage causes retrograde amnesia and affects all senses.
evolution
All primates have visual area 5.
Middle superior temporal region {optical flow field} {middle superior temporal area} (MST) encodes motion perception, especially texture flows.
Lateral temporal regions {non-medial temporal region} can include polar region, inferotemporal area, and posterior parahippocampus and retrieve factual knowledge, but not skill, perception, or motor control.
Region near hippocampus {parahippocampal area} includes rhinal cortex, with medial temporal lobe memory system and multisensory convergence. Parahippocampal area region {parahippocampal place area} responds most to places, not objects.
Cortex near nose {perirhinal cortex} damage causes inability to consciously remember facts or events, such as new category members or unique examples. Damage does not affect perceptual-motor skills with no conscious internal representations, such as mastering task over several sessions or retrieving previously acquired factual knowledge.
Posterior inferior temporal region {posterior inferotemporal cortex} (PIT) receives from ventral-pathway area V4 and sends to anterior inferotemporal cortex. Attention affects it [DeWeerd et al., 1999].
Posterior superior temporal regions {posterior superior temporal lobe} can be at temporal-occipital-parietal junction, be for associative memory, and retrieve representations and concepts [Bruce et al., 1986].
Posterior temporal-lobe regions {posterior temporal lobe} can be for consonant strings, words, speech fluency, and categorical knowledge. Visual association area-18, area-19, and posterior-area-37 bilateral damage prevents unique object recognition and feature retrieval.
Right temporal lobe region {right temporal lobe} controls spatial relationships, form manipulations, and visual discriminations.
Superior temporal lobe gyrus {superior temporal gyrus} represents sounds.
Superior temporal lobe sulcus {superior temporal sulcus} (STS) detects head or face movement, separate from viewing angle or recognition. Anteriorly, in area V4 and V4A, it analyzes color and color constancy. It detects shapes and textures. Posterior cingulate, medial frontal gyrus, and superior temporal sulcus are about imagining how other people feel.
Temporal regions {V6 temporal brain area} {area V6, temporal lobe} can be for locations.
Ventral temporal-lobe regions {ventral temporal lobe} can control attention and consciousness.
Central brain spaces {ventricle, brain}| are down middle, hold cerebrospinal fluid, and connect to spinal cord fluid tube. Beneath septum pellucidum, first two ventricles connect through hole to third ventricle, which is between right and left hypothalamus lobes. Tectum covers third ventricle in back. In front of third ventricle are septal and preoptic areas. Fourth ventricle is in hindbrain.
Fourth-ventricle aqueduct {cerebral aqueduct} is in midbrain.
Almost transparent tissue {septum pellucidum}, in cerebrum beneath corpus callosum, separates first and second ventricles.
Forebrain neural activities can correlate with sense qualities {neuronal correlates of consciousness}| (NCC) [Alauddin et al., 2003] [Calvin, 1996] [Calvin, 1996] [Calvin, 1998] [Cotterill, 1998] [Changeux, 1983] [Crick and Koch, 1992] [Crick and Koch, 2003] [Crick, 1979] [Crick, 1994] [Dehaene and Changeux, 2004] [Dehaene and Naccache, 2001] [Dehaene, 2001] [Dehaene et al., 2003] [Dragunow and Faull, 1989] [Fried et al., 1998] [Graziano et al., 2002] [Greenfield, 1995] [Greenfield, 2000] [Han et al., 2003] [Jasper, 1998] [Koch and Davis, 1994] [Koch, 2004] [Lechner et al., 2002] [Li et al., 2002] [Llinás et al., 1998] [Slimko et al., 2002] [Taylor, 1998] [Yamamoto et al., 2003].
brain processes
Consciousness is not about brain processes, because they are at low level. Algorithm high-level code must use low-level code for processor. Brain processes do not yet reveal higher code or algorithm.
brain regions
Consciousness can be a whole-brain, many-connected-region, few-connected-regions, or one-brain-region property [Chalmers, 2000] [Metzinger, 2000] [Mollon and Sharpe, 1983] [O'Regan and Noë, 2001] [Pessoa et al., 1998] [Teller, 1984] [Teller and Pugh, 1983].
Perhaps, brain has sets of different neurons, whose information, interactions, or processing is necessary and/or sufficient for consciousness aspects.
Awakeness depends on nuclei below cortex and thalamus that excite, or remove inhibition from, cortex and thalamus non-specifically, but these nuclei do not directly make sense qualities.
Sense qualities depend on cortex and thalamus, but cortex and thalamus regions project to local or distant cortex and thalamus locations, so no region relates to sense qualities.
complexity
Many non-conscious processes involve complex computations, and brain can learn complex non-conscious processes. Many widespread brain processes have no association with consciousness. Both unconscious and conscious processes involve neurons with high firing rates and/or large chemical changes.
feedback
Perhaps, consciousness requires feedback in brain pathways. Illusions can switch between two different sense qualities or perceptions about same figure or image. Perception depends on memory and thalamocortical feedback.
iteration
Perhaps, experience involves iteration, but repetition delays processing and limits discrimination.
Probably, experience does not use iteration, repetition, waves, vibrations, oscillations, or anything periodic, because such processing limits information.
mind requirements
Consciousness requires information from objects and events outside brain, information transfer from receptors to processors, and effector controls. Information channels from objects and events to brain to effectors must have enough information capacity and speed. Channels have reverse channels to provide feedback and synchronization. Information codes must express all physical relations.
physiology
Perhaps, cell membrane polarizations and depolarizations; chemical concentration changes from manufacture, destruction, or transfer; or cell structure changes at synapses or dendrites have biochemical and biophysical effects that cause experience. Perhaps, brain-pathway cellular-connection changes cause experience. Consciousness-causing activity must last long enough to allow integration and be short enough to prevent signal overlap. Neuron activity affects other neurons, so correlations can be widespread and indirect.
similar neurons
Perhaps, brain has "consciousness neurons" that have similar ion channels, shapes, receptors, axons, synapses, and/or biochemistry. Perhaps, some neuron feature is necessary and/or sufficient for consciousness aspects. However, no neuron properties or events, including connections, directly relate to sense qualities.
Testing visual nerve pathways {visual pathways} can reveal neural activity related to visual sense qualities. Consciousness uses brain regions for attention, shape, and planning and goals [Chalmers, 2000] [Ffytche, 2000] [Kanwisher, 2001] [Lumer, 2000] [Lumer et al., 1998].
Scientists know visual pathways better than other sense pathways [Andersen et al., 1990] [Baizer et al., 1991] [Barbas, 1986] [Felleman and Van Essen, 1991] [Karnath, 2001] [Kennedy and Bullier, 1985] [Lewis and Van Essen, 2000] [Maunsell and Van Essen, 1983] [Rockland and Pandya, 1979] [Saleem et al., 2000] [Salin and Bullier, 1995] [Van Essen and Gallant, 1994] [Zeki and Shipp, 1988].
visual pathway level 01
Level 01 is from Retina to Lateral Geniculate Nucleus [LGN]. Damage affects sight, but processing is not sufficient for consciousness. Though retinal-cell distribution causes lower visual acuity outside fovea, sense qualities do not seem to have much lower acuity. Only two color-receptor types are in fovea, but sense qualities seem to have all colors. Few color receptors are outside fovea, but sense qualities seem to have all colors. Though retina has blind spot, people do not notice it. Eye movements can cause fuzziness, but sense qualities do not show much blurring. Blinking can cause darkness, but sense qualities are not black then.
visual pathway level 02
Level 02 is LGN, in Thalamus, to area V1. Damage affects sight, but processing is not sufficient for consciousness. LGN modulates stimuli received from retina, so it does not determine sense qualities, because retina does not.
visual pathway level 03
Level 03 is Superior Colliculus [SC] to LGN. Damage does not affect sight. SC just controls saccades.
Level 03 includes Pulvinar Nucleus and other brainstem nuclei to areas V1, V2, and SC. Damage does not affect sight. Brainstem nuclei just control gaze, pupil size, blinking, and daily rhythms.
Level 03 includes area V1 or Brodmann 17, in dorsal and ventral pathways, to areas V2, V3, PIP, V3A, PO, V4t, V4, MT, and MSTl. Damage affects sight, but processing is not sufficient for consciousness. Area V1 codes motions and objects separately, but these unite in sense qualities. People do not use V1 in dreams, which have sense qualities. V1 neuron responses stay the same when ambiguous-figure sense qualities alternate. V1 neuron responses can change with unconscious blinking, eye movement, and fast color alternation, though sense qualities stay the same.
visual pathway level 04
Level 04 is area V2, V2 dorsal [V2d], and V2 ventral [V2v], in dorsal and ventral pathways, to areas V3, VP, PIP, V3A, PO, V4, V4t, VOT, VIP, MSTd, MSTl, FST, and FEF. Damage affects sight, but processing is not sufficient for consciousness. V2 codes shape, contrast, depth, motion, edges, and figure separately, but these unite in sense qualities.
visual pathway level 05
Level 05 includes areas V3, V3 dorsal [V3d], and V3 ventral [V3v] in dorsal pathway to PIP, V3A, PO, MT, V4t, V4, VIP, LIP, MSTd, FST, FEF, and TF. Processing is not sufficient for consciousness. V3 codes for fast response, not object images.
Level 05 includes Ventral Posterior [VP], in ventral pathway, to PIP, V3A, PO, MT, V4, VOT, VIP, LIP, FST, FEF, and TF. Processing is not sufficient for consciousness. VP neuron responses reflect both retinal stimulation and sense qualities.
Level 06 includes Posterior Intraparietal [PIP] and Posterior Parietal complex [PPcx], in dorsal pathway, to PO, MT, V4, DP, and 7a. Processing is not sufficient for consciousness. PIP just controls attention.
visual pathway level 06
Level 06 includes V3A, in ventral pathway, to PO, MT, V4, DP, LIP, MSTd, MSTl, FST, and FEF. Processing is not sufficient for consciousness. V3a codes only for shape, but sense qualities include other features.
Level 07 includes Medial Dorsal Parietal [MDP], in dorsal pathway, to PO and 7a. Processing is not sufficient for consciousness. MDP codes for fast response, not object images.
visual pathway level 07
Level 07 includes Medial Intraparietal [MIP], Intraparietal dorsal [IPd], and Intraparietal anterior [IPa], in dorsal pathway, to PO and 7a. Processing is not sufficient for consciousness. MIP codes for fast response, not object images.
Level 07 includes Parietal-Occipital [V6] [PO], PO anterior [POa], PO anterior-internal [POa-i], PO anterior-external [POa-e], Lateral Occipital Parietal [V7] [LOP], Lateral Occipital Caudal [LOC], and Dorsal Medial Occipital complex [DMOcx], in dorsal pathway, to MDP, MIP, MT, V4t, DP, VIP, LIP, MSTd, MSTl, 7a, and FEF. Processing is not sufficient for consciousness. PO codes for fast response, not object images.
Level 07 includes Medial Temporal [V5] [MT], MT caudal [MTc], Temporal A [TA], TA anterior [TAa], Temporal E [TE], TE anterior [TEa], TE medial [TEm], TE antero-dorsal [TEa-d], TE antero-ventral [TEa-v], TE anterior-medial [TEa-m], TE1, TE2, TE3, TE1-3, TE1-3 dorsal [TE1-3d], TE1-3 ventral [TE1-3v], and Temporal E Occipital [V8] [TEO], in dorsal and ventral pathways, to PO, V4t, V4, VIP, LIP, MSTd, MSTl, FST, FEF, 46, and Prefrontal. Processing is for objects. Most neurons are about perception.
Level 07 includes V4 transitional [V4t], V4t anterior [V4ta], and V4t posterior [V4tp], in ventral pathway, to PO, MT, V4, MSTd, MSTl, FST, and FEF. Cells can track sense qualities and unsensed alternative-figure perception.
Level 07 includes V4, in ventral pathway, to MT, V4t, DP, VOT, LIP, FST, PITd, PITv, FEF, CITd, CITv, AITv, 46, TF, and TH. Cells can track sense qualities and unsensed alternative-figure perception.
visual pathway level 08
Level 08 includes Dorsal Prelunate [V7] [DP], in dorsal pathway, to LIP, MSTd, MSTl, FST, 7a, FEF, and 36. Processing is not sufficient for consciousness. DP codes for fast response, not object images.
Level 08 includes Ventral Occipital Temporal [V8] [VOT], Occipital Temporal A [OA], and OA anterior [OAa], in ventral pathway, to PITd and PITv. Processing is for space.
visual pathway level 09
Level 09 includes Ventral Intraparietal [VIP], VIP*, VIP lateral [VIPl], and VIP medial [VIPm], in dorsal pathway, to LIP, MSTd, MSTl, FST, 7a, and FEF. Processing is not sufficient for consciousness. VIP codes for fast response, not object images.
Level 09 includes Lateral Intraparietal [LIP], LIP dorsal [LIPd], and LIP ventral [LIPv], in dorsal pathway, to VIP, MSTd, MSTl, FST, 7a, FEF, 46, and TF. Processing is not sufficient for consciousness. LIP codes for fast response, not object images.
Level 09 includes Medial Superior Temporal dorsal [MSTd], MSTd anterior [MSTda], and MSTd posterior [MSTdp], in dorsal pathway, to VIP, LIP, FST, PITd, PITv, 7b, 7a, FEF, STPp, and TF. Processing is not sufficient for consciousness. MSTd codes for fast response, not object images.
Level 09 includes Medial Superior Temporal lateral [MSTl], MST medial [MSTm], and MST complex [MSTcx], in dorsal pathway, to VIP, LIP, FST, 7a, FEF, and STPp. Processing is not sufficient for consciousness. MSTl codes for fast response, not object images.
Level 09 includes Floor of Superior Temporal [FST], Ventral Superior Temporal [VST], and VST complex [VSTcx], in ventral pathway, to VIP, LIP, MSTd, MSTl, PITd, PITv, 7a, FEF, STPp, and TF. Processing is for space.
Level 09 includes Posterior Inferior Temporal dorsal [PITd] and Inferior Temporal complex [ITcx], in ventral pathway, to FST, PITv, FEF, CITv, AITd, AITv, and 46. Cells track whether sensation is on or off.
Level 09 includes Posterior Inferior Temporal ventral [PITv], in ventral pathway, to FST, PITd, FEF, CITd, CITv, AITd, AITv, TF, and TH. Cells track whether sensation is on or off.
visual pathway level 10
Level 10 includes Brodmann 7b [7b], in dorsal pathway, to 7a, STPp, and 36. Processing is not sufficient for consciousness. 7b codes for fast response, not object images.
Level 10 includes Brodmann 7a [7a] and 7a lateral, in dorsal pathway, to 7b, FEF, STPa, AITd, 36, 46, TF, and TH. Processing is not sufficient for consciousness. 7a codes for fast response, not object images.
Level 10 includes Frontal Enterofrontal [Brodmann 8] [FEF], in dorsal and ventral pathways, to 7a, STPp, CITd, CITv, AITd, and 46. FEF integrates fast responses and object perception.
Level 10 includes Superior Temporal Parietal posterior [STPp], Temporal-parietal [Tpt], Temporal-Parietal-Occipital [TPO], TPO caudal [TPOc], TPO intermediate [TPOi], TPO rostral [TPOr], Parietal Temporal G [PG], and PG anterior [PGa], in dorsal and ventral pathways, to 7b, FEF, CITd, CITv, STPa, 46, TF, TH, Striatum, and Prefrontal. Processing is for space, shape, and texture, but STPp has no topographic maps.
Level 10 includes Caudal Inferior Temporal dorsal [CITd], in ventral pathway, to FEF, STPp, AITd, AITv, 46, and TH. Processing is for shape and texture, but STPp has no topographic maps.
Level 10 includes Caudal Inferior Temporal ventral [CITv], in ventral pathway, to FEF, STPp, AITd, AITv, 46, TF, and TH. Processing is for shape and texture, but STPp has no topographic maps.
visual pathway level 11
Level 11 includes Superior Temporal Parietal anterior [STPa], in dorsal and ventral pathways, to AITd, 36, 46, TF, TH, 35, ER, Striatum, and Prefrontal. Processing is for shape and texture, but STPp has no topographic maps.
Level 11 includes Anterior Inferior Temporal dorsal [AITd], in ventral pathway, to STPa, 36, 46, TF, TH, Striatum, and Prefrontal. Processing is for shape and texture, but STPp has no topographic maps.
Level 11 includes Anterior Inferior Temporal ventral [AITv], in ventral pathway, to STPa, 36, 46, TF, TH, 35, HC, Striatum, and Prefrontal. Processing is for shape and texture, but STPp has no topographic maps.
visual pathway level 12
Level 12 includes Brodmann 36 [36], in dorsal pathway, to Brodmann 46, TF, TH, 35, ER, and HC. Processing is not sufficient for consciousness. Brodmann 36 codes for fast response, not object images.
Level 12 includes Brodmann 46 [46], in dorsal and ventral pathways, to Brodmann 36, TF, TH, and ER. Brodmann 46 integrates fast responses and object perception.
Level 12 includes Temporal F [TF], in ventral pathway, to Brodmann 36, 46, and ER. Processing is about high-level object perception.
Level 12 includes Temporal H [TH], in ventral pathway, to Brodmann 36, 46, and ER. Processing is about high-level object perception.
visual pathway level 13
Level 13 is Brodmann 35 [35], in dorsal pathway, to ER. Processing is not sufficient for consciousness. Brodmann 35 codes for fast response, not object images.
visual pathway level 14
Level 14 is Entorhinal area [ER], in dorsal and ventral pathways, to HC. ER integrates fast responses and object perception.
visual pathway level 15
Level 15 includes Hippocampus [HC], in dorsal and ventral pathways. HC integrates fast responses and object perception. Processing is for memory.
Spinal nerve tracts {spinal cord}| organize basic movements, like running or walking, and control sense input. Spinal cord has inner gray matter cell bodies and outer white matter myelin, in lemnisci.
laminas
Lamina V is for pain and visceral afferents. Lamina VI is for joints and skin positions. Lamina VIII is medial motor neuron column for motor neurons to trunk and limbs. Lamina IX is lateral motor neuron column for motor neurons to arms and legs, with flexor central and extensor peripheral. Lamina X is central canal.
locations
Pain, heat, and cold axon tracts are on spinal-cord lateral sides. Touch and pressure axon tracts are on ventral side. Muscle-sensor axon tracts are on dorsal side.
Axons and dendrites can mix {neuropil}.
Spinal cord has outer white matter {lemnisci} with fascicles grouped into funiculi columns.
Spinal-cord outer white matter has descending and ascending axon tracts {fascicle} grouped into lemnisci.
Spinal-cord lamina I {Lissauer's tract} {Lissauer tract} is for pain.
Spinal-cord dorsal-horn lamina II {substantia gelatinosa} receives touch, pressure, pain, and thermal sensations.
Spinal-cord laminas {lamina III} can be for position and light touch.
Spinal-cord laminas {lamina IV} can be for position and light touch.
Spinal-cord laminas III and IV {nucleus proprius} are for position and light touch.
Spinal-cord laminas {lamina VII} {dorsal nucleus} {Clarke's column} can have intermediolateral nucleus and be for preganglion sympathetic system.
Spinal-cord lamina-VII dorsal nucleus ganglion {intermediolateral nucleus} contains preganglion sympathetic neurons.
Spinal-cord nerve tracts {medial longitudinal fasciculus} can be for head and eye coordination and come from vestibular nuclei.
Spinal-cord tracts {reticulospinal tract} can modulate sensation and spinal reflexes.
Spinal-cord tracts {rubrospinal tract} can be motor.
Spinal-cord back horn {dorsal horn} is for sense input and has ascending sense-connector nerves.
functions
Dorsal column is for fine touch and proprioception from skin, tendon, and joint.
layers
Dorsal horn has five layers. Layer 1 receives axons from skin neurons and sends to neurons higher in spinal cord. Layers 2 and 3 modulate sense input from both skin neurons and neurons in layers 4 and 5. Layer 4 receives axons from skin neurons and sends axons to layer 5. It detects gentle and general pressures. Layer 5 receives axons from skin, viscera, and layer-4 neurons and sends to brain.
nuclei
Neuron nuclei {dorsal column nuclei} receive afferent fibers from skin and send to ventrobasal complex.
tracts
Tracts are spinothalamic tract, dorsal spinocerebellar tract, ventral spinocerebellar tract, and spinoreticular pathway.
neurons
Nociceptive-specific neurons respond to noxious stimuli. Wide dynamic range neurons respond to all mechanical stimuli, but especially to noxious mechanical or thermal stimuli.
Spinal-cord front horn {ventral horn} is for motor output and has descending motor nerves. Tracts are lateral corticospinal tract, anterior corticospinal tract, vestibulospinal tract, rubrospinal tract, reticulospinal tract, and tectospinal tract. Descending autonomic neurons come from hypothalamus and brainstem. Medial longitudinal fasciculus is for head and eye coordination and comes from vestibular nuclei.
Voluntary escape behaviors use small efferent spinal cord fibers with long latencies and variable responses, which react to visual, tactile, and vibratory threats.
Spinal cord and brain have connective tissue layers {meninges}|, dura mater, pia mater, and arachnoid. Cerebrospinal fluid is between layers and in central canal.
Spinal cord has inner connective tissue layer {arachnoid}.
Spinal cord has outer connective tissue layer {dura mater}.
Spinal cord has middle connective tissue layer {pia mater}.
Cells {neuron} can have cell body, dendrites sending signals in, and axon carrying signals out.
shapes
Surroundings and connections cause unique neuron shapes. Large named neurons with special shapes include spinal cord anterior horn cells, cerebellum Purkinje cells, lateral vestibular Deiters cells, teleost Mauthner cells, primate cerebral cortex Betz cells, and primate cerebral cortex Meynert cells. Mauthner cells are for escape and startle reflexes.
size
Neurons are largest human cells, with average diameter 20 microns. Neuron volume is thousand times larger than bacterium volume.
firing rate
Neurons can output signals at maximum rate {rate saturation, neuron}, different for different neurons, up to 900 per second.
neuron genes
100 different neuron types express different gene sets. 80% of genes have repression, and the other 20% have expression at different levels, varying with cell conditions and transcriptional control. 20% of genes are for transcriptional control [Keller, 2000] [Stevens, 1998].
individuality
Neurons are different, because brains have hundreds of neurotransmitters and neurohormones, such as amino-acid derivatives, peptides, and small RNAs. Neurons have different membrane-receptor, membrane-polarization, myelination, microtubules, and gene-expression patterns. Neurons differ temporally, with different responses over different time scales. Interactions cause neurons to act differently [Grush and Churchland, 1995] [Shepherd, 1991].
One neuron {command neuron} can code for complex functions {single neuron doctrine}, because it responds to feature set [Calvin and Ojemann, 1994] [Kreiman et al., 2000] [Kreiman, 2001] [Kreiman et al., 2002] [Ojemann et al., 1998]. For example, after training, neurons can respond preferentially to face, hand, or object aspects.
problems
Number of brain neurons is not large enough to account for all possible objects and views. Neurons do not seem to converge on one brain area. Convergence is slow process, but pattern-representation formation is fast. Researchers have not found brain command neurons. Single cells cannot change efficiently in response to environment or body changes.
Dendrite proteins {cytoplasmic polyadenylation element binding protein} {CPEB protein} can bind to polyA regions, have active and inactive states, build other synapse proteins, and affect other protein shapes.
Neuron extracellular-potential changes have minor electrical effects {ephaptic interaction} on other neurons [Holt and Koch, 1999].
Neuron output depends on product of various inputs {gain field}. Outputs combine neuron population codes.
Neuron can output continuously variable electrical potential {graded potential} rather than impulse.
A microelectrode {neuronography} can stimulate one nerve.
Neurons have reflexes, ON-center neurons, other neuron types, ganglia, orientation columns, topographic maps, association cortex, and memory systems {neuron assembly}.
reflexes
Brain can modify reflexes. Inhibition from controllers and excitation from motivators compete to cause behavior or fading.
ON-center and OFF-center neurons
ON-center and OFF-center neurons detect points and lines. ON-center and OFF-center neuron arrays can detect point and line arrays and so textures, boundaries, and objects.
neuron types
Besides ON-center neurons, other neuron types detect color and other intensities.
orientation columns
Cortical orientation columns detect line and boundary orientations and detect angles and so detect surface orientations.
topographic maps
Ganglia and topographic maps code relations among perceptions and motions.
association cortex
Association cortex controls series and parallel perceptual and motor systems, integrating information to guide behavior.
memory systems
Cortical systems have three-dimensional registers to hold spatial perceptual information temporarily and permanently.
The main fiber {axon}| from soma is thin and smooth cylinder with neurofilaments. It is conductive. It has same-size branches at obtuse angles. It has bulbous endings and/or calyciform endings. It has small varicosities in chains. It has no ribosomes. It attracts specific dendrites.
Chemical flow in both directions supplies axon ends with molecules from cell body.
number
Most neurons have one axon. Retinal amacrine and olfactory granule cells have no axons. Dorsal root ganglion cells have multiple axons and no dendrites. Dorsal root ganglion cells have axon that bifurcates. Invertebrate cells often have one axon, with dendrites from it.
microtubule
Only axon hillock and initial segment have microtubule fascicles, have membrane undercoating, and have high sodium-channel density.
excitation or inhibition
Axon terminals are either all excitatory or all inhibitory.
regeneration
Axons can regenerate, if allowed by surrounding glial cells.
Axon initial segment {trigger zone} {axon hillock}| has many sodium channels and allows action potential to trigger.
If axon disrupts, Nissl substance changes appearance {chromatolysis} over 4 to 12 weeks.
Microtubules and neurofilaments {cytoskeleton} make cell and axon framework.
Wide filament protrusions {dendrite}| from soma have synapses for axons.
anatomy
Dendrites have microtubules. Dendrites do not myelinate or have one myelin layer.
shape
Branching dendrites provide maximal surface area for receiving input from other neurons. Larger diameter and/or shorter length make larger effects on initial segment.
Proximal and distal dendrites are different.
Widespread dendrites receive from many sources. Compact dendrites receive from one source.
Dendrites can radiate straight out in all directions with few spines, as in large ventral-horn motor cells and reticular-formation cells. They can branch with spines curving in one direction, as in cerebral-cortex pyramidal cells and secondary sense nuclei. They can have special patterns and locations. Cerebellar Purkinje cells are planar semicircles. Inferior-olive clustered cells are curved and wavy. Ventral-cochlear nucleus cells are tufted. Smaller branches are at acute angles and have thorns.
Dendrite patterns match incoming axon patterns. Branches orient along body axes, brain surfaces, and nerve bundles.
Dendrites can change shape over days.
main
Cell body typically has several dendrite origins {basal dendrite}. Cerebellar Purkinje cells have one dendrite trunk {apical dendrite}. Dorsal-root ganglion cells have no dendrites. Invertebrate cells often have one axon, with dendrites from it.
properties
Dendrites have high resistance and capacitance. At dendrite ends, membrane is relatively unexcitable.
If stereotyped behavior happens over four to five months, dendrites from several antagonistic motor neurons make a bundle {dendritic bundle}.
Dendritic protrusions {dendritic spine} have asymmetric synapses. Spines vary in shape, size, and density, even on one dendrite. They can change shape over days. One dendritic spine has only one Type 1 synapse but can also have one Type 2 synapse. Spines have alpha-tubulin, beta-tubulin, actin, and myosin filaments. They have endoplasmic reticulum. Excitation is at spine tips. Inhibition is at dendritic bases or on cell surface. More spines indicate more excitation.
All animals have synapses {electrical synapse} {gap junction, synapse} that use ion flows in one direction and are excitatory or inhibitory [Beierlein et al., 2000] [Blatow, 2003] [Gibson et al., 1999].
function
Electrical synapses make adjacent cells fire at same time. Cortex interneuron groups link by electrical synapses and can act together to inhibit.
comparison
Electrical synapses are faster but less efficient than chemical synapses, with signal one-quarter original signal. For example, if presynaptic membrane is 100 mV, post-synaptic membrane is 25 mV.
properties
Electrical synapses cannot have facilitation and do not change shape.
Sodium, potassium, calcium, and chloride have passageway {ion channel, neuron}| through membrane protein. Ion channel for receptor potential differs from ion channel for action potential [Doyle et al., 1998] [Heinemann et al., 1992] [Hille, 2001].
Synapses {Malsburg synapse} {von der Malsburg synapse} can rapidly control connectivity between cells, allowing transient cell assemblies.
Lipids {myelin}| can increase axon conduction rates and separate nerve fibers. Schwann cells in PNS, and oligodendrocytes in CNS, make myelin. Schwann cells measure neuregulin in axons and make more myelin if it is higher and less if it is lower. Myelination begins in brain lower back after birth and moves toward frontal lobes, finishing about age 25. Myelin can have up to 150 layers. Conduction is fastest when axon diameter to total diameter is 0.6.
Neuron membrane sites {neuroreceptor} bind molecules.
types
Neuroreceptors include alpha-adrenergic catecholamine such as alpha2-adreneric, AMPA, angiotensin, beta-adrenergic catecholamine, D1, D2, GABA, glycine, kainate, M, metabotropic, muscarinic ACh, N, and NMDA receptors.
hormone
Hormone binds to cell-membrane outer-surface neuroreceptor protein, which opens membrane channel for up to one second. On cell-membrane inner surface, neuroreceptor protein couples to G protein and activates adenylate cyclase, guanylate cyclase, phospholipase c, or phosphoinositidase C, which produces soluble cAMP, cGMP, or phosphoinositide second messenger, which diffuses into neuronal cytoplasm and changes local membrane potential.
Cyclic nucleotide or phosphoinositide can either stimulate or inhibit other enzymes. ADP triphosphoinositide {phosphatidylinositol 4,5 diphosphate} hydrolyzes to release water-soluble inositol triphosphate (IP3) (ITP), which releases calcium ion from intracellular storage, which initiates enzyme phosphorylation. Phosphoinositidase C hydrolysis makes diglyceride containing arachidonic acid, which, with calcium and phospholipid, activates protein kinase C.
neurotransmitter
A 10-nanometer-wide glycoprotein channel spans cell membrane and activates by neurotransmitter. Activation allows ions to flow through channel down concentration gradient. Sodium ions flow from outside to inside membranes. Potassium ions flow from inside to outside membranes. Chloride ions flow from outside to inside membranes. Channel opens for only one microsecond, because neurotransmitter rapidly dissociates or inactivates.
Ribosome clumps {Nissl body}| {Nissl substance} are in rough endoplasmic reticulum cisterns. If axon disrupts, Nissl substance changes appearance {chromatolysis, Nissl substance} over 4 to 12 weeks.
Points {Ranvier node} {node of Ranvier}| along myelinated axon have no myelin. Conduction jumps from node to node. Beside node, which has sodium channels, is paranode, which has juxtaparanode, which has potassium channels, beside it.
Neurons have cell bodies {soma} {perikaryon}.
Protein discs {postsynaptic density} (PSD) are on presynaptic and postsynaptic chemical-synapse membranes. PSDs have beta-adrenergic, glutamate, and gamma-aminobutyric acid (GABA) receptors. They have protein kinase enzymes that phosphorylate to alter synaptic structure. They contain filamentous proteins that can move and change shape, such as actin, actin/calmodulin-binding protein, fodrin or brain spectrin, and tubulin. Fodrin or brain spectrin is an actin-binding and calmodulin-binding protein.
Axon terminal synapses have hexagonal grids {presynaptic grid}, with six particles surrounding each vesicle.
Cell enzyme produces soluble cyclic nucleotide, cAMP or cGMP, or phosphoinositide {second messenger}|, which diffuses into neuronal cytoplasm and changes local membrane potential.
Axons connect to dendrites at chemical sites {synapse}|. Neuron activity, habituation, and sensitization affect synapses. With more activity, number of synapses per neuron increases, synapse density per unit volume rises, and dendrite length increases. Neuroactive compounds exert influence up to 20 nanometers within synaptic cleft or up to 2 millimeters from varicosities or unstructured release points [Gray, 1977].
In synapses, space {synaptic cleft}| between membranes is 20 nm wide and has acidic and basic glycoproteins and mucopolysaccharides, with dense line in middle, that bind membranes. Synaptic cleft is bigger in asymmetric synapses.
Cortical axons have ending arrays {arborization} {synaptic terminal}| with total diameter 0.5 millimeters, containing 2000 boutons and synapses.
Presynaptic areas have membrane sacs {synaptic vesicle}| {vesicle} with neurotransmitter molecules. Vesicles contain only one transmitter type.
types
Clear synaptic vesicles contain acetylcholine, glycine, GABA, glutamate, aspartate, or neurohormones. Vesicles with granule in middle contain dopamine, noradrenaline, adrenaline, or serotonin. Larger granular vesicles contain peptides.
transmitters
Adrenal chromaffin cells store opiate peptides and catecholamines. Sympathetic neurons and neuromuscular junctions store ATP and other transmitters. Hypothalamic magnocellular neurons store vasopressin and oxytocin. Autonomic neurons store acetylcholine and VIP or norepinephrine Y.
biology
One spike releases one packet. Vesicle containing acetylcholine has 1000 to 10,000 molecules. Vesicles contact cell membrane, because time is less than 200 microseconds between first calcium entry and first neurotransmitter in synapse.
Excitatory synapses {asymmetric synapse} {Type 1 synapse} can have postsynaptic density, round vesicles, and wide clefts and connect mainly to dendritic spines.
Inhibitory synapses {symmetric synapse} {Type 2 synapse} can have small and narrow synaptic clefts, ellipsoidal or flattened vesicles, and no postsynaptic density and connect mainly to dendritic shafts and cell bodies.
Neuron axons can have long chains of swellings {varicosity}, which are similar to synapses and release neurotransmitter from their surfaces near dendrite terminal branching regions.
Neurons attach {neuron adhesion} {neural attachment} symmetrically at zonula adhaerens, punctum adhaerens, zonula occludens, and nexus. Neurons have no macula adhaerens or desmosome.
Neurons adhesions {punctum adhaerens} attach symmetrically.
Neurons attach symmetrically at chemical synapses {zonula adhaerens}.
Neurons attach symmetrically between epithelial or endothelial cells {zonula occludens} {tight junction}.
Neurons make electrotonic synapses {nexus, synapse}.
Electrotonic synapses have membrane proteins {connexon} for ion transmission.
Neurons have physiology {neuron, physiology}.
signals: initiation
Neurotransmitter reception reduces membrane voltage. Membrane voltage reduction spreads. At axon hillock, membrane voltage can reach threshold voltage, causing depolarization spike, which initiates depolarization-spike traveling wave down axon.
Perhaps, only one dendrite-and-cell-body membrane potential distribution can cause initiation. Only one distribution can reach threshold potential. One distribution has much higher probability than others, because it can happen in the most ways. Dendrite and cell body changes can change distribution. Perhaps, neuron groups also detect only one input distribution.
signals: firing rate
Neuron input to neuron-firing rate ratio is linear or S-shaped.
conduction rate
Non-myelinated-axon conduction rate is between 0.5 and 2 meters per second, 1 millimeter per millisecond. Myelinated-fiber conduction rate is between 2 and 120 meters per second, 10 millimeters per millisecond, and is faster because signals jump from one Ranvier node to the next {saltatory conduction, myelin}.
Conduction rate in axons varies irregularly.
Faster impulse conduction became necessary as animals became larger.
conduction rate: synapse
Conduction rate across synapse is one micrometer per millisecond. Irregular synapse sizes and neurotransmitter-packet release times vary conduction rate.
Post-synaptic decay takes up to ten milliseconds.
conduction rate: synchronization
Information-flow rates along axons, synapses, and receptors change typically do not synchronize with rates on other axons, synapses, and receptors.
neuron growth
Neurons grow, differentiate, migrate, and extend axons and dendrites, at different rates. Extracellular substances, cell-membrane molecules, and cell and axon spatial arrangements affect growing axons. Cell-membrane-molecule and extracellular-substance gradients change over time. Target neurons grow and mature in coordination with axon growth.
neuron growth: direction
Adhesion-glycoprotein neurotrophins guide growing nerve processes to appropriate target neurons.
neuron growth: process
First, several axons travel over relatively short distance. After axons stop extending, they produce multiple branches, which form many connections. Branch retraction and synapse reduction then reduce connections. First nerve impulses, which are possibly synchronous, refine axon connections [Thompson, 1940] [Wolpert, 1977].
nutrition
Nerve cells need glucose and oxygen, because they have no substitute biochemical pathways.
plasticity
Neuron number, spatial arrangements, diameters, composition, lengths, types, controllers, molecules, membranes, axons, dendrites, cell bodies, receptors, channels, synapses, threshold voltages, and packet number can change. Receptor number, type, effectiveness, and position can change.
plasticity: repair
After brain damage, nearby axons invade damaged region to make new circuits, and axons try to contact nearby dendrites.
Unconditioned stimulus (UCS) releases serotonin from axon to axon synapses {axoaxonic synapse}, which increase protein kinase A, which releases more glutamate. Association is non-Hebbian.
Cutting axons {axon cutting} makes neuron die and nearby axons sprout processes to innervate neuron dendrites that used to contact dead neuron.
Proteins, lipids, and neurotransmitters travel 300 mm/day {axon transport}|, away from cell soma. Mitochondria travel 75 mm/day, away from cell soma. Actin microfilaments, glycolytic enzymes, myosin-related polypeptides, calmodulin, and clathrin travel 5 mm/day, away from cell soma. Microtubules and neurofilaments travel 1 mm/day, away from cell soma. Lysozyme breakdown products travel 250 mm/day, back to cell soma. Fast transport uses ATP and kinesin protein along microtubules.
Depolarization increases glutamate binding to NMDA receptor, which activates pathways {CREB pathway} to increase cyclic AMP, which increases CREB protein, which increases transcription of genes that make synapses larger and more efficient.
Neurotransmitter packets reaching post-synaptic cell-membrane neuron receptors cause small voltage differences, positive {excitation} {hyperpolarization} or negative {inhibition} {depolarization}|. Sodium ions diffuse into cell, and potassium ions diffuse out, causing voltage change across cell membrane. Voltage change spreads to nearby cell membrane.
Depolarization increases glutamate binding to NMDA receptor, which activates CREB pathway to increase cyclic AMP, which increases CREB protein, which increases transcription of genes that make synapses larger and more efficient.
In sympathetic autonomic ganglia, presynaptic cholinergic fibers excite one neuron class with acetylcholine and another class with LHRH-like peptide, which diffuses several micrometers to make slow excitatory postsynaptic potential {excitatory postsynaptic potential} (EPSP).
Neuron-axon back projections can cause long-term membrane depolarization {facilitation}|.
Most reflex responses decrease {habituation}| if non-threatening stimulus repeats without reinforcement. Receiving same stimulus repeatedly or continuously decreases sensation.
purpose
Habituation allows animal to ignore persisting situation or disregard irrelevant stimuli.
specific
Habituation is only to specific stimulus. Habituation ends immediately when stimulus pattern changes. Therefore, dishabituation can detect if animal perceives anything new.
behavior
Sexual behavior can have habituation.
timing
Habituation happens sooner the second time. Habituation happens sooner to weak stimuli.
time
In mammals, habituation decreases receiving-neuron post-synaptic potential for up to one hour. Because back-projection signals decrease, calcium influx is lower, sending neuron releases less transmitter, and receptor alters.
In marine snails, decreased vesicle release, from sense to motor neurons, causes habituation that persists for minutes. Repeated habituation decreases presynaptic-terminal number.
comparison
Tiredness does not cause habituation. Habituation cannot be for associative learning.
Senses have absolute intensity differences {just noticeable difference}| (JND) {difference threshold}, between two stimuli, that people can perceive. Stimulus intensity ratio typically ranges from one to three but can be up to sixty.
For fast millisecond effects, neurotransmitter receptors have ion channels {ligand-gated ion channel}. Fast neurotransmitters include acetylcholine and glutamate.
If climbing fiber depolarizes Purkinje cell, parallel fibers make nitrogen oxide, which increases cGMP in Purkinje cell, which activates protein kinase G, which makes receptors less sensitive {long-term depression} (LTD).
Dendrite spine synapses can have long-lasting changes {long-term potentiation} (LTP).
process
Presynaptic glutamate release activates N-methyl-D-aspartate (NMDA) postsynaptic receptors, causing Ca++ entry into postsynaptic neurons, which activates calcium/calmodulin protein kinase II (CaM kinase II), protein kinase C, and/or tyrosine kinase, which changes spine shape, synapse shape, or receptors. Perhaps, CaM kinase II adds AMPA receptors to postsynaptic membrane. Spine shape alteration exposes NMDA receptors and changes spine electrical properties. Short spine neck has high electrical resistance that amplifies depolarization. Lengthening neck permits increased Ca++ influx.
time
High-frequency hippocampus or cortex nerve stimulation increases synapse depolarization for hours {early LTP}, and, if repeated, up to weeks {late LTP}.
purposes
LTP aids space representation and affects spatial memory.
protein
Cell-membrane binding integrin protein maintains long-term potentiation and so aids memory.
locations
In hippocampus, Schaffer collateral pathway, from hippocampus region CA3 pyramidal cells to hippocampus region CA1, uses glutamate, is associative, and has post-synaptic NMDA receptor modulation. Hippocampus region CA3 pyramidal cells receive from dentate gyrus. Mossy fiber pathway, from dentate gyrus granule cells to hippocampus region CA3, uses glutamate, is non-associative, has norepinephrine interneuron modulation, and seems not to affect declarative memory. Dentate-gyrus granule cells receive from entorhinal cortex.
Regular low-frequency stimulation causes presynaptic bulb hypopolarization {low-frequency depression} (LFD) and decreases post-synaptic neuron output.
Acetylcholine can bind to slow neurotransmitter receptors {muscarinic ACh receptor}.
Adult bird, primate, and human brain neural stem cells divide to form neural precursors and new neural stem cells {neurogenesis}. Neurogenesis increases with brain activity.
Drugs, learning, growth, disease, accident, mutation, hormones, and chance can alter neuron properties {plasticity}|. Brains can change structure in response to stimuli and so learn [Petit and Ivy, 1988] [Robertson, 2000].
After binding a neurotransmitter packet of 1000 to 10,000 molecules, post-synaptic membrane changes 1 mV to 15 mV {post-synaptic potential} (PSP), with average of 10 mV, lasting 10 to 100 milliseconds. Initial change is rapid, and decay is slow. Potential change affects membrane up to two millimeters away. Spontaneous neurotransmitter release makes changes of 0.5 mV, lasting 20 milliseconds. Miniature end plate potentials depolarize synapse by 0.7 mV, lasting 10 milliseconds. Frequency is directly proportional to membrane depolarization. Frequency is five per second at membrane resting voltage.
Regular high-frequency stimulation causes presynaptic bulb hyperpolarization {post-tetanic potentiation} (PTP) and increases post-synaptic neuron output.
All cells in all organisms have receptor potentials and action potentials {potential gradient}, caused by sodium-ion, potassium-ion, and chloride-ion concentration gradients across cell membranes. All cells have potential changes, as ions move through membrane channels. Neurons require energy to maintain ion balance across membranes.
In excitatory axons, conditioned stimulus (CS) allows calcium to enter axon terminal and release glutamate {presynaptic facilitation}. Unconditioned stimulus (UCS) releases serotonin from axon-to-axon axoaxonic synapses, which increase protein kinase A, which releases more glutamate. Association is non-Hebbian. More UCS also activates MAP kinase and expresses genes to make more glutamate synapses.
In excitatory axons, unconditioned stimulus inhibits presynaptic bulb {presynaptic inhibition}.
Brain activity leaves trace {priming, nerve}, making path more easily excitable next time. Priming lasts tens to hundreds of milliseconds. Priming sets or sequences {context, priming} last minutes or hours.
Conscious states last 100 to 150 milliseconds {psychological refractory period}, same time it takes to make or perform decisions. Perhaps, after sending feedforward signal, brain sends no more signals for refractory period, to allow time to check first-signal results.
Inactive periods {refractory period, neuron}|, 0.75 milliseconds to 4 milliseconds, follow neuron spikes at axon positions, as membrane returns to normal voltage.
Receptor size and information processing method determine smallest size {resolution} that sense can detect. For example, eye can see 1 arc-second or 0.000001 meter, microwave size. Wavelengths longer than microwaves are not good for vision because spatial resolution is poor.
In myelinated fibers, conduction rate is between 2 and 120 meters per second or 10 millimeters per millisecond, as signal jumps {saltatory conduction, myelinated fiber}| from one Ranvier node to the next. Conduction rate along all axons varies irregularly.
Neurotransmitter binding to synapse receptors reduces membrane voltage, which spreads to axon hillock. When membrane voltage reaches threshold at axon hillock, cell membrane has large and rapid voltage change {spike, axon}| [Koch, 1999] [Salinas and Sejnowski, 2001] [Softky, 1995].
level
Spike voltage rises from -70 mV to +5 mV in 0.5 millisecond and then falls back to -70 mV in 0.5 millisecond.
time
Depolarizations have short duration, allowing precise time and time-interval coordination and comparison.
strength
Depolarizations have same strengths and time intervals. Depolarization prevents nerve-signal deterioration with distance and time, allowing axons to be long and act over long time intervals. Neurons can thus be anywhere and have any pattern.
threshold
Threshold can vary, between -50 mV and -30 mV.
Depolarization makes neurons act like switches. Threshold keeps neurons off until they switch on. Rapid recovery makes them switch off.
Computers are switching networks and can change switch thresholds.
Switches can contain messages in binary code [Adrian, 1980].
travel
Depolarization brings adjacent cell membrane to threshold, causing adjacent spike. That spike, in turn, causes adjacent cell membrane to reach threshold, causing adjacent spike. Spikes travel along axon from axon hillock to synapse.
direction
Spikes cannot go backward because cell membrane takes time to recover from spike. Ions at previous-spike cell membrane have low concentration and do not flow across membrane.
rate
Axons can sustain up to 800 spikes per second. Spikes cannot repeat faster at a cell-membrane location, because cell membrane takes 0.5-millisecond refractory period to recover from a spike.
factors
Axon hillocks do not distinguish neurotransmitters, receptors, or input patterns. All things that effect membrane voltage merely add.
Neurotransmitter synapse effects can be fast and short or slow and long {synaptic transmission}.
For fast millisecond effects, neurotransmitters, such as acetylcholine and glutamate, bind to receptors with ligand-gated ion channels.
For slow 0.1-second to 10-second effects, neurohormones, such as dopamine, acetylcholine, and neuropeptides, bind to receptor that activates GTP-binding proteins {G-protein}, which make second messengers such as cyclic AMP, diacylglycerol (DAG), or inositol triphosphate (IP3), which phosphorylate.
Stimuli can cause neuron sets to fire simultaneously {synchronization}, 40 to 100 milliseconds after stimulus. Neurons with overlapping same-type receptive fields have the most synchrony. Synchronous neuron activity is always in phase, not in opposite phase. Synchronous neuron signals do not encode information about space, objects, or time.
High-frequency electrical stimulation causes maximum nerve signaling {tetanus, nerve}|.
Cell membrane has voltage {threshold, neuron} at which it starts depolarization spike. Low threshold allows too much noise. High threshold cuts off boundary effects, shading, and small differences.
absolute
Senses have smallest detectable stimulus {absolute threshold}, which people can sense 50% of time. For vision, humans can detect light if seven photons flash in absolute darkness. For hearing, humans can detect whisper at five meters in absolute silence. For touch, humans can detect small insect wing or foot in still air. For smell, if small perfume drop is in ballroom, air is still, and no other odors are present, humans can detect perfume. For taste, humans can detect four grams of sugar in one liter of water.
Presynaptic cholinergic neurons excite peripheral sympathetic neurons {trans-synaptic enzyme induction}.
Neuron and glia molecules cause nerve growth {trophism}|, guide axon tips to final locations during development, regulate and maintain nervous-system connections, and stimulate neurotransmitters.
At receptor, catecholamine agonist causes desensitization {tolerance, regulation}, because agonist receptors have reduced affinity and subsequently decrease in number {down-regulation}. Down-regulation persists for days after transmitter concentrations have returned to normal {temporal amplification, down-regulation}.
Denervation, catecholamine depletion, or catecholamine antagonist treatment causes suprasensitivity {up-regulation}, because receptor number increases. Up-regulation persists for days after transmitter concentrations have returned to normal {temporal amplification, up-regulation}.
Motor neurons {alpha motor neuron} can initiate movement by stimulating muscles.
Brain has many small nerve cells {amacrine cell, neuron} {microneuron}, which inhibit other neurons in memory and other processes. Amacrine cells have 27 types and send to the ten inner-plexiform layers.
Cerebellum neurons {basket cell} can receive excitation from parallel fibers and laterally inhibit adjacent-column Purkinje cells. Axons go one millimeter away and form multiple synapses on cell bodies and dendrites. Basket cells make GABA for inhibition.
Brain has elongated neurons {bipolar cell, neuron} of 10 types that send to the ten inner plexiform layers.
Medial entorhinal cortex and para-subiculum have 10% cells {border cell} that fire when viewing a nearby border.
Brain neurons {chandelier cell} can inhibit pyramidal cells with multiple synapses at axon base. Chandelier cells make GABA for inhibition.
Basal nucleus of Meynert, medial septal nucleus, and brainstem nuclei neurons {cholinergic neuron} can make acetylcholine and alter in Alzheimer's disease, ALS, and spinal cord injury.
Visual-cortex cells {complex cell} can receive from simple cells and ganglion cells. Complex cells have ocular dominance or orientation tuning.
functions
They can detect stereoscopic effects, such as line-segment ends, colors, motions, and line orientations. They can mark region boundaries, such as regions with same reflectance. They discriminate and aggregate. They can detect patterns, at any location.
fields
Complex cells have different receptive-field sizes and detect different spatial frequencies and so widths. Sets can detect 8 to 30 different frequency bands and spatial scales, using spatial frequency channels, from pixel, spot, region, quadrant, or whole visual field.
time
Complex-cell sets can operate at 10 to 30 different temporal scales, from milliseconds to years.
Edge neurons {double-bouquet cell} can make GABA to inhibit other-edge-side vertical-column activity.
Simple cells can detect line or bar ends {end-stopped inhibition} {end stopping, simple cell} or detect no end. End-stopping cells increase firing rate, as bar length increases up to maximum, and then decrease firing rate, as bar gets longer.
Neurons {excitatory neuron} can excite other neurons.
types
They are either bursting {bursting cell} or non-bursting. They cannot change from one type to the other.
bursting
Bursting cells respond to sustained intracellular current with two to four spikes, followed by hyperpolarization, followed by burst, followed by hyperpolarization, and so on, with 0.2 to 10 cycles per second.
Bursting cells are large. Apical dendrites extend to layer 1 to contact many cells. Axons project to ipsilateral superior colliculus.
Bursting neurons accumulate calcium more efficiently in axon terminals than cells that have isolated spikes.
Layer-5 bursting neurons induce synaptic plasticity in neurons outside cortex. Spike bursts turn on short-term memory, which then decays over several seconds.
non-bursting
Non-bursting neurons, such as pyramidal or spiny stellate neurons, have one spike or sustained output. They do not have spike cycles.
Interneurons {GABA neuron} {GABA+ neuron} can have no dendrite spines {smooth neuron, GABA}. They affect epilepsy and Huntington's disease [Koch, 1999] [Lytton and Sejnowski, 1991] [McBain and Fisahn, 2001].
Motor neurons {gamma motor neuron} can control muscle length/tension relationships, by exciting nearby alpha motor neurons and stimulating muscle sensors.
Retinal output neurons {retinal ganglion cell} {ganglion cell, retina output}| generate action potentials and have axons in optic tract to brain [Enroth-Cugell and Robson, 1984] [Meister, 1996] [Niremberg et al., 2001] [Warland et al., 1997].
biology: types
Ganglion cells are magnocellular M, parvocellular P, and mixed W, which process signals separately and send separate information streams to lateral geniculate nucleus (LGN).
Retinal ganglion cells {X-cell} {beta retinal ganglion cell} can sum linearly across receptive fields. X cells have large dendritic fields. X-cells resolve finer visual patterns with higher spatial frequencies. X cells make tonic and sustained signals, with slow conduction, for detecting details and spatial orientation. More X cells are in fovea. X cell axons go to simple cells.
Magnocellular cells respond better to motion, respond better to transient stimulation, respond better to small intensity differences, are larger, have larger receptive fields, have thicker axon with faster signals, have firing rate that plateaus only at high intensity, and signal scene changes.
Retinal ganglion cells {Y-cell} {alpha retinal ganglion cell} can sum non-linearly. Y cells have small dendritic fields. Y-cells are larger and have thicker and faster conducting axons. Y cells make phasic and transient signals, with fast conduction, for stimulus size and temporal motion. More Y cells are in periphery. Y cell axons go to complex cells.
Parvocellular cells have several types, have better spatial resolution, detect color, detect higher contrast, detect more detail, are more numerous, and have more linear responses.
Both X-cells and Y-cells have ON-center and OFF-center neurons. X-cells and Y-cells have different receptive field sizes, stimulus velocity sensitivities, and spatial frequencies.
Retinal ganglion cells {W cell} can be small and direction sensitive, with slow conduction speed. W cells mix M and P cell properties and are rarest.
biology: neuron shapes
Ganglion cells {bistratified neuron} {small bistratified neuron} can have two dendrite layers. Cells {shrub neuron} can have dendrite bushes.
Ganglion cells look like auditory nerve cells, Purkinje cells, olfactory bulb cells, olfactory cortex cells, and hippocampal cells.
biology: input
Small central-retina midget ganglion cells have small dendrite clump, to collect signals from one midget bipolar cell. Midget cells respond mostly to contrast.
Parasol ganglion cells can receive from diffuse bipolar cells with bigger dendrite trees and can have dendrite umbrella, to collect signals from wide area. Parasol cells respond mostly to change.
biology: output
Ganglion cells send to LGN and then to cortical hypercolumn.
functions
Visual-receptor cells take illumination logarithm and hyperpolarize 0 mV to 4 mV from resting level 10 mV to 30 mV [Dowling, 1987] [Enroth-Cugell and Robson, 1984] [Wandell, 1995]. Retinal ganglion cells sum bipolar, horizontal, and amacrine retinal-neuron activities. Retinal ganglion cells have low spontaneous-firing rate. Ganglion cells typically respond quickly and then turn off.
Retinal ganglion cells make action potential after cyclic GMP reduces, decreasing sodium conductance through cell membrane.
functions: spots
Retinal ON-center ganglion cells can respond when light intensity above background level falls on center of their receptive field. See Figure 1. Light falling on annulus surrounding receptive-field center inhibits cell.
When light smaller than center falls on center, ON-center neuron fires rapidly and then slowly. After removing light, ON-center neuron continues low firing rate. When light smaller than annulus falls on annulus, ON-center neuron does not fire. After removing light, ON-center neuron fires rapidly and then slowly.
ON-center neurons have four types, depending on excitation and inhibition. One has high firing rate at onset and zero rate at offset. One has high rate, then zero, then high, and then zero. One has high rate at onset, goes to zero, and then rises to constant level. One has high rate at onset and then goes to zero.
Other ganglion cells {OFF-center neuron} respond when light intensity below background level falls on receptive-field center. OFF-center neurons increase output when light intensity decreases in receptive-field center. Light falling on annulus around receptive-field center excites OFF-center cells.
When light smaller than center falls on center, OFF-center neuron does not fire. After removing light, OFF-center neuron fires rapidly and then slowly. When light smaller than annulus falls on annulus, OFF-center neuron fires rapidly and then slowly. After removing light, OFF-center neuron continues low firing rate.
Bipolar cells excite ON-center and OFF-center neurons. ON-center and OFF-center neurons compare light intensity falling on receptive-field center with that falling on annulus.
functions: bars
Band, bar, stripe, grating, or edge excites ON-center neuron in different ways.
If grating has wide stripes, ON-center neuron has only spontaneous firing, because one bright band affects both center and surround, exciting and inhibiting. See Figure 2.
If grating has narrow stripes, ON-center neuron has only spontaneous firing, because several bright bands affect both center and surround, exciting and inhibiting. See Figure 3.
If grating-stripe width lands on center exactly, ON-center neuron fires rapidly and then slowly. See Figure 4.
For wide single long bar, ON-center neuron has only spontaneous firing, because bright band affects both center and surround. See Figure 2.
For narrow single long bar, ON-center neuron has some firing, because bright band affects mainly center but is small. See Figure 5.
If long bar lands exactly on center, ON-center neuron fires rapidly and then slowly. See Figure 4.
For long bar with end beyond center, ON-center neuron has only spontaneous firing, because bright band affects both center and surround. See Figure 5.
For short bar with end not yet at center, ON-center neuron has only spontaneous firing, because bright band does not reach center. See Figure 6.
For bar with end on center {end stopping, neuron}, ON-center neuron fires rapidly and then slowly. See Figure 7.
For bright edge over center, ON-center neuron fires rapidly and then slowly. See Figure 8.
For bright edge not yet at center, ON-center neuron has no firing. See Figure 9.
For bright edge at middle, ON-center neuron fires some. See Figure 10.
If grating-stripe width lands on center exactly, ON-center neuron fires rapidly and then slowly. See Figure 4.
If grating-stripe width shifts to half on and half off, ON-center neuron fires some. See Figure 10.
If grating-stripe width shifts to all off, ON-center neuron does not fire. See Figure 9.
For bright or dim regions, ON-center neurons have only spontaneous firing, because bright light affects both center and surround.
For bright or dim regions, OFF-center neurons have only spontaneous firing, because bright light affects both center and surround. Relative brightness depends on lateral-inhibition patterns.
functions: movement
Ganglion cells {ON-OFF-center neuron} can detect movement. ON-OFF-center neurons use time derivative of ON-center neurons to find general direction and position. Amacrine cells also excite transient ON-OFF-center neurons.
functions: color
Retinal ganglion cells can be cone-shaped cells for color detection. The three types compare light intensities in frequency range. Type is for brightness, adds green and yellow-green, and has both on-center and off-center neurons. Another type has center for one cone color and surround for another color, to compare colors. Third type, with no surround, adds green and yellow-green for excitation and subtracts blue for inhibition, to compare blue to yellow.
Cerebellum has clusters {glomerulus, cerebellum} {glomeruli, cerebellum} of 20 granule cells.
Cerebellum neurons {Golgi cell} can be in granule-cell layer. Golgi cells receive input from parallel, mossy, and climbing fibers. They inhibit granule cells to provide feedback and feedforward inhibition. They change parallel fiber activity into brief burst.
Neurons {Golgi type I neuron} {local circuit neuron} can send locally with unmyelinated axons.
Neurons {Golgi type II neuron} {projection neuron} can send to other areas with myelinated axons.
Golgi cells inhibit cerebellum neurons {granule cell}. One mossy fiber excites 20-granule-cell clusters {glomerulus, granule cell} {glomeruli, granule cell}.
Medial entorhinal cortex has some cells {grid cell} that fire when body is at many spatial locations, which form a triangular grid [Sargolini et al., 2006].
Post-subiculum, retrosplenial cortex, anterior thalamic nuclei, lateral dorsal thalamic nuclei, lateral mammillary nucleus, dorsal tegmental nucleus, striatum, and entorhinal cortex have some neurons {head direction cell}, which receive from vision and vestibular systems, that fire only when head has an orientation in space [Sargolini et al., 2006].
Superficial pyramidal cells {hypercomplex cell} can detect corners, depths, and lengths.
Neurons {inhibitory neuron}| that inhibit other neurons fire faster than excitatory neurons, have few spines on dendrites {smooth neuron, inhibition}, and synapse directly on dendrites, cell bodies, or dendritic stumps, closer to axon hillock than excitatory axons. Inhibitory axons connect horizontally, only up to 100 to 200 microns away, except for basket cells.
Large spindle-shaped neurons {spindle neuron} {Korkzieher cell} are only in great-ape anterior-cingulate and frontal-area-FI lower layer 5, for output to other regions [Economo and Koskinas, 1925] [Nimchinsky et al., 1999]. Humans have them in much higher densities than other apes. They form after birth. Spindle neurons are for attention and self-reflection. Layer 6 has small spindle-like cells.
People have three million nerves {motor nerve} {motor neuron} to muscles and glands. Alpha motor neurons can initiate movement by stimulating muscles. Gamma motor neurons can control muscle length/tension relationships by exciting nearby alpha motor neurons and stimulating muscle sensors. Internuncial neurons can allow reciprocal inhibition.
input
Cerebrum, basal ganglia, brainstem, and cerebellum act on motor neurons. Impulse excitatory effect on motor neuron lasts 5 milliseconds.
regeneration
Motor nerves can regenerate connections to muscles.
Brain neurons {multipotent neural stem cell} can divide regularly to make neural stem cells and neural precursors. Half of neural precursors migrate, then mature into neurons or glia. Migration and maturation take one month.
Neurons {neural stem cell} can make five neuron types: TH+ neurons, GABA+ neurons, cholinergic neurons, astrocytes, and oligodendrocytes. Neural stem cells are mainly in ventricles and hippocampus. They can migrate to hippocampus and olfactory bulbs.
Excitatory neurons {pyramidal cell}| can connect one cortical area to another and fire in bursts. Pyramidal cells are both superficial and deep [Elston, 2000] [Elston and Rosa, 1997] [Elston and Rosa, 1998] [Elston et al., 1999].
functions
Pyramidal cells detect fast moving stimuli, such as moving edge at one orientation.
output
Cerebral cortex layer-5 pyramidal cells send to thalamic nuclei, mainly to lateral geniculate nucleus and inferior, lateral, and medial pulvinar nuclei. Half of layer-6 pyramidal cells send to lateral geniculate nucleus, and others send to claustrum, hippocampal system, and anterior cingulate sulcus motor-system higher planning levels. Pyramidal cells with short dendrites, not reaching into layer 1, send to other cerebral cortex regions. Excitatory extrinsic axons come from pyramidal cells. Pyramidal cells also send to local neurons using axon collaterals.
Pyramidal cells inhibit stellate cells. Pyramidal-cell to stellate-cell ratio is two to one.
processing
Pyramidal cells have high spontaneous activity and large receptive fields. Sustained intracellular current causes high-frequency action potentials {regular spiking cell}, which decrease within 50 to 100 milliseconds.
All vertebrate sense cells {sensory cell} developed from ectothelial cell type.
Visual-cortex cells {simple cell} can receive from lateral geniculate nucleus (LGN) ON-center and OFF-center neurons. Simple cells receive from both eyes but process one eye faster and so have ocular dominance. Simple cells have more precise tuning than LGN or retinal cells. See Figure 1.
lines
Cells that compare ON-center and OFF-center neuron superpositions can find boundaries and heighten contrasts. Simple cells can detect lines, edges, stripes, or gratings. Simple cells can detect 12 to 30 line, edge, stripe, or grating orientations {orientation tuning, cell}. Simple cells have different receptive field sizes and detect different line, edge, stripe, or grating spatial frequencies and widths.
color
Some simple cells detect color.
movement
Some simple cells detect movement.
arrays
Simple cells have arrays in topographic maps. See Figure 2.
Neurons {smooth stellate cell} can send only to superficial and deep pyramidal cells.
Neurons {spiny stellate cell} can send only to superficial and deep pyramidal cells. Spiny-stellate-cell inhibitory axons connect horizontally only up to 100 to 200 microns away.
Cortical layer-4 cells {stellate cell} can detect bars, slits, and edges, in static pictures, at 20 orientations. Stellate cells have small receptive fields and low spontaneous activity. Smaller stellate cells excite easier. Cerebellum stellate cells receive excitation from parallel fibers and laterally inhibit adjacent-column Purkinje cells.
Neurons {superficial pyramidal neuron} can send unmyelinated collaterals, with no terminal branches, sideways to tight terminal clusters. Neurons repeat this for many millimeters: every 0.43 mm in primary visual cortex, every 0.65 mm in secondary visual areas, every 0.73 mm in sensory strip, and every 0.85 mm in monkey motor cortex. Macrocolumns of similar emphasis connect by synchronizing excitation.
Brain output neurons {tufted cell} can be secondary.
Neurons {TH+ neuron} can make serotonin and affect Parkinson's disease.
Nerve chemicals {neural chemical} {nerve chemical} are hormones, ions, modulators, receptors, regulators, transmitters, and structures.
transverse motion
Only biological cells use transverse ion motion to make depolarization wave. If axon has nodes of Ranvier, depolarization jumps from node to node and transverse ion motion is same strength in all directions around axon circumference. If axon has no nodes of Ranvier, transverse ion motion is all around axon circumference but is most at least-resistance point. Ions repel each other, so differences are small. Depolarization waves travel down lines on axon surfaces, following least-resistant path, and can spiral down axon.
Calcium ions move from mitochondria and endoplasmic reticulum through channels {calcium ion channel} onto receptors. Calcium ions phosphorylate synapsin proteins and cause vesicle fusion with membrane, to trigger neurotransmitter release. Calcium ions clear from receptors by active transport back into mitochondria and endoplasmic reticulum.
Dendrite voltage-gated Ca++ channels can provide non-linear coupling between inputs.
Transmitter-gated calcium-ion channels are like other channels {P/Q-type calcium channel}.
Serotonin and cyclic AMP regulate calcium-ion entry into cells, including neurons.
Cells have chloride-ion channels {chloride ion channel}.
Cells have seven potassium-ion channel types {potassium ion channel}.
cAMP mediated receptors {S channel} close potassium-ion-channel type. cAMP mediated receptors reduce a potassium-ion-channel size, to allow longer action potentials and allow more calcium ion to flow into presynaptic area and increase transmitter release.
Cells have sodium-ion channels {sodium ion channel}.
Brain neurons secrete chemicals {neurohormone} that affect other neurons more slowly than neurotransmitters. Neurohormones can cause signal pattern from neuron group [McEwen, 1976].
Circulating vasoconstrictor molecules {angiotensin} can bind to presynaptic noradrenergic nerve terminals. Kidney renin enzyme changes angiotensinogen to angiotensin.
Bone proteins {bone morphogenetic proteins} regulate whether neural precursors become neurons or glia.
Brain releases peptides {bradykinin} in response to injury to stimulate neurons.
Hormones {brain-derived neurotrophic factor} (BDNF) can increase NMDA-receptor phosphate binding and can develop immature sympathetic and sense neurons and glia.
Most endocrine-hormone or neurotransmitter gastrointestinal-system peptides {gut-brain peptide} {brain-gut peptide} {brain-gut axis} are also brain hormones or neurotransmitters. Most gastrointestinal system peptide receptors are also in brain. Brain and gut peptides include bombesin, cholecystokinin (CCK), gastrin, motilin, neurotensin, pancreatic polypeptide, secretin, substance P, and vasoactive intestinal peptide (VIP).
Medullary-motor-nuclei transmitters {calcitonin-gene-related peptide} (CGRP) can regulate phenotypic expression.
brain peptide {carnosine}.
Glycoproteins {neurotrophin} {cell adhesion molecule} (CAM) {axon guidance molecule} can guide growing nerve processes to appropriate target neurons. Hormones develop immature neurons and glia. For example, neurotrophin-3 increases oligodendrocyte number. 1,1-CAM protein helps begin myelination.
Peptides {cholecystokinin} (CCK) can cause satiation by binding to solitary tract nucleus (NTS) receptors, enhances dopamine actions, and is in gut, cerebral cortex, medulla oblongata, solitary tract nucleus, and ventral midbrain.
Hormones {ciliary neurotrophic factor} (CNTF) can decrease immature neuron and glia death and supports eye ciliary-ganglion parasympathetic neuron survival. Perhaps, CNTF is survival or trophic factor, mitogen, or transmitter-regulating factor for other neurons.
Brain hormones {circulating hormone}, such as angiotensin, calcitonin, glucagon, and insulin, can release into blood.
Three genetically different endorphin peptide families are proopiomelanocortin (POMC), proenkephalins, and prodynorphin {dynorphin}. Dynorphin peptides act like opioids. Gut, posterior pituitary, hypothalamus, basal ganglia, and brainstem make prodynorphin. Leucine-enkephalin leads to dynorphin. Dynorphin in nucleus accumbens neurons inhibits VTA neurons and so reduces dopamine.
Hormones {galanin} can be in basal forebrain and hypothalamus.
Brain and gut peptide hormones {gastrin}| can control stomach secretion.
Hormones {glial growth factor-2} (GGF-2) can increase glia number.
Hormones {glial-derived neurotrophic factor} (GDNF) {glial cell line-derived neurotrophic factor} can make new axon branches in motor neurons.
Hormones {gonadotropin-releasing hormone} can release gonadotropin in hypothalamus.
Hormones {growth-hormone-releasing hormone} can release growth hormone in hypothalamus.
Hypophysis makes oxytocin, neurophysins, and vasopressin {hypophyseal hormone} {neurohypophyseal hormone}.
Hormones {hypothalamic releasing hormones} can release hormones, such as growth-hormone-releasing, gonadotropin-releasing, and luteinizing-hormone-releasing hormones, from hypothalamus.
Hormones {insulin-like growth factor} (IGF-1) can help develop immature neurons and glia.
Peptides {kyotorphin} can act as opioids.
Hormones {lipotropin} can be from pituitary.
Norepinephrine, epinephrine, dopamine, and serotonin {monoamine}| are slow-acting neuromodulators, come from brainstem, and affect arousal and sleep.
Peptides {motilin} can be in gut and cerebellum.
Hormones {nerve growth factor} (NGF) can go into sympathetic-neuron and sense-neuron axon terminals and transport to cell body, where it increases transmitter levels. Olfactory bulb, cerebellum, and striatum make nerve growth factor and nerve growth factor receptor.
enzyme
In hippocampal neurons, NGF increases choline acetyltransferase (CAT), which synthesizes acetylcholine and can reverse poor spatial memory.
disease
NTRK1 gene makes neurotrophin tyrosine kinase receptor type 1. NTRK1 gene mutation causes rare autosomal recessive disease (CIPA) with pain insensitivity, no sweating, self-mutilation, fever, and mental retardation.
Molecules {netrin} attract and repel axons to guide axon directions.
Peptides {neuropeptide} can have high concentrations in nervous-system regions and low concentrations in other cells and organs. Neuropeptides include brain-gut peptides, circulating hormones, hypothalamic releasing hormones, neurohypophyseal hormones, opioid peptides, pituitary hormones, bradykinin, carnosine, epidermal growth factor (EGF), neuropeptide Y, proctolin, and substance K. Brain hormones, such as opioids, act slowly [McEwen, 1976].
Peptides {neuropeptide Y} (NPY) can be in cerebral cortex and medulla oblongata. Arcuate-nucleus appetite region sends neuropeptide Y to second appetite region.
Hypophysis makes nerve hormones {neurophysin}.
Steroids {neurosteroid} can induce sleep, be analgesic at high concentration, and come from cholesterol or progesterone.
Peptides {neurotensin} can be in gut, hypothalamic arcuate nucleus, medulla oblongata, retina, solitary tract nucleus, and ventral midbrain.
Hormones {notch growth factor} can regulate whether neural precursors become neurons or glia.
Macrophages make protein {oncomodulin} that regenerates nerve.
Peptides {pancreatic polypeptide} can be in brain and gut.
Peptides {peptide hormone}, such as endorphins and enkephalins, can produce slower effects than neurotransmitters and come from 20% of inhibitory cells. Enzymatic hydrolysis inactivates such peptides, so they do not reabsorb into synaptic terminals or glial cells [McEwen, 1976].
Pituitary hormones {pituitary hormone} are alpha melanocyte-stimulating hormone (alpha MSH), corticotropin (ACTH), growth hormone (GH), lipotropin, luteinizing hormone, prolactin, somatotropin, and thyrotropin.
Hormones {presenilin} can decrease neural stem-cell division.
Peptides {proctolin} can be in brain.
Peptides {secretin} can be in brain and gut.
Molecules {semaphorin} can attract and repel axons to guide axon directions.
Thalamus, cortex, and hippocampus hormones {somatostatin} (SS) can mimic hypothalamus sympathetic-neuron substance-P regulation. Somatostatin treats diabetes.
Hormones {somatotropin} can be in pituitary.
Hormones {sonic hedgehog growth factor} {sonic hedgehog gene} can regulate immature-neuron cell division. Sonic hedgehog gene activates pathway that affects central-nervous-system development.
Peptides {substance K} can be in brain.
Proteins {survival motor neuron proteins} can preserve motor neurons.
Chemicals {neuroregulator} {neuromodulator} can amplify or negate neurotransmitters by altering transmitter-receptor interactions, changing ion flux, or activating neuroreceptor enzymes.
Molecules {ampakine} increase glutamine binding to AMPA receptor and increase glutamate release from AMPA receptor, affecting memory and cognition.
Molecules {diacylglycerol} (DAG) can phosphorylate ion channels.
Molecules {inositol triphosphate} (IP3) can phosphorylate ion channels.
Proteins {alpha-integrin} can bind to cell membranes, maintain long-term potentiation (LTP), and aid memory.
Enzymes {protein kinase Mz} can be necessary and sufficient for long-term potentiation.
Chemicals {retrograde messenger} can diffuse back from postsynaptic to presynaptic membrane. For example, upon protein-kinase activation, nitric oxide synthase makes nitric oxide from l-arginine. Nitric oxide diffuses back from postsynaptic to presynaptic membrane and causes increase in vesicle release, if membrane is still active.
Proteins {beta-adrenergic catecholamine receptor} {beta-receptor} {adrenergic catecholamine} can bind catecholamines. Binding couples to G protein and adenylate cyclase metabolism. Beta-receptor protein strongly binds ISO, binds epinephrine, and weakly binds norepinephrine. Binding can cause vasodilation, uterine contraction inhibition, cardiac stimulation, and bronchodilation. If guanosine triphosphate (GTP) is present, beta-receptors have only low-affinity catecholamine binding.
Proteins {agrin} can cluster other proteins between neurons and muscle cells and at immune synapses.
Sympathetic noradrenergic nerve terminal proteins {alpha-receptor}, such as alpha-2 receptor, bind to norepinephrine strongest, epinephrine middle, and isoproterenol (ISO) lowest. Binding can cause vasoconstriction, uterine contraction, and mydriasis. Alpha-receptor agonist and alpha-receptor antagonist affect alpha-receptors.
Proteins {AMPA receptor} {aspartate receptor} can bind aspartate, glutamate, and glutamine. Binding is fast, opens sodium ion channels, and causes excitation.
Proteins {angiotensin II receptor} can bind angiotensin in presynaptic noradrenergic nerve terminals.
Neuron receptors {autoreceptor} can be on presynaptic membranes, for negative feedback.
Nociceptors {cannabinoid receptor} (CB1) can have cannabis receptors. Anandamide, 2-arachidonoyl glycerol (2-AG), and marijuana delta-9-tetrahydrocannabinol (THC) bind in hypothalamus, basal ganglia, amygdala, brainstem, hippocampus, cerebellum, and neocortex. Hypothalamus affects appetite, sex, and hormones. Basal ganglia affect motor acts and planning. Amygdala affects emotion, anxiety, and fear. Brainstem affects pain and reflexes. Hippocampus affects memory and learning. Cerebellum affects motor acts. Neocortex affects sense qualities and cognition.
2-AG flows from receptor cell back to transmitting cell to decrease GABA {depolarization-induced suppression of inhibition} (DSI) [Earleywine, 2002] [Grinspoon and Bakalar, 1993].
immune
CB2 receptor is only in immune system.
Proteins {CD45 protein} can be for synapse and immune-synapse adhesion.
Proteins {D1 receptor} {D1 dopamine receptor} {dopamine D1 receptor} can bind dopamine. Binding is slow, uses cAMP, opens potassium ion channels, closes calcium ion channels, and inhibits.
Proteins {D2 receptor} {D2 dopamine receptor} {dopamine D2 receptor} can bind dopamine. Binding is slow, uses cAMP, opens potassium ion channels, closes calcium ion channels, and inhibits.
Dopamine receptors {DRD4 dopamine receptor} can be in brain. Perhaps, DRD4-gene allele {attention-deficit hyperactivity disorder, dopamine} arose 40,000 years ago and allowed bolder and more-curious personalities.
Receptor complexes {GABA receptor} {gamma-aminobutyric acid receptor} can bind GABA.
types
Type A {GABA-A receptor} is fast, opens chloride-ion channels, and inhibits. Type B {GABA-B receptor} is slow, opens potassium-ion channels, closes calcium-ion channels, uses IP3 and DAG, inhibits, and uses second-messenger system, probably cyclic AMP.
parts
Endogenous benzodiazepine-receptor protein is part of GABA-receptor complex and increases extent or period of GABA-operated chloride-ion channel opening.
drugs
Benzodiazepines and anxiety-reducing neuromodulators {anxiolytic drug, GABA} increase GABA affinity for GABA neuroreceptors and enhance GABA-mediated synaptic potentials. Perhaps, anesthetics bind to GABA-A. Perhaps, neurosteroids from progesterone and cholesterol bind to GABA-A.
Proteins {glycine receptor} can bind glycine. Binding is fast, opens chloride-ion channels, and inhibits. Dorsal-horn neurons have glycine receptors for inhibition. ACEA competitively blocks glycine receptor. Strychnine affects glycine receptor. Prostaglandins block glycine receptors and so excite dorsal horn neurons.
Outer-membrane receptors {G-protein-coupled receptor} (GPCR) can have seven alpha helices in cell membrane and has active protein part inside cell membrane next to G protein. For example, olfactory sense neurons have membrane receptors that activate G protein. For slow 0.1-second to 10-second effects, receptor activates G protein, which binds GTP to make second messengers such as cyclic AMP, diacylglycerol (DAG), or inositol triphosphate (IP3), which phosphorylate ion channels.
Ion channels {ionotropic receptor} {transmitter-gated ion channel} can bind neurotransmitters, such as glutamine, and then open quickly. Response to ion flows is 10 to 30 times faster than metabolotropic response.
Proteins {kainate receptor} can bind glutamate. Binding is fast, opens sodium ion channels, and excites.
Proteins {M receptor} can bind acetylcholine. Binding is slow, opens calcium ion channels, excites or inhibits, and uses IP3, cAMP, or DAG.
Neurotransmitters, such as glutamate, can bind to receptors {metabotropic receptor}, which affect G protein, which activates adenyl cyclase, which changes ATP to cAMP, which binds to cAMP-dependent protein-kinase regulatory subunit, which affects catalytic subunit, which phosphorylates protein, which opens or closes ion channels, which increases calcium ion. Such receptors amplify signals 100-fold and cause cell-effect patterns.
factors
Calcium ion and other second messengers affect cAMP activity. Metabolism uses IP3 and DAG.
speed
Response to neurotransmitter-neuroreceptor activation is 10 to 30 times slower than ionotropic response.
Proteins {mGluR5 receptor} can bind glutamate and affect cocaine dependence.
Acetylcholine receptors {muscarinic ACh} can use second messenger.
Proteins {N receptor} can bind acetylcholine. Binding is fast, opens sodium ion channels, and excites.
Cell membranes between two neurons or immune cells can form tubes {nanotube, cell} that can transfer calcium, proteins, or viruses.
Protein receptors {neuropilin} can be at synapses and immune synapses.
Nicotine is similar to acetylcholine. Immune cells and neural cells have acetylcholine receptors. Nicotine inhibits cytokine release by macrophages. Proteins {nicotinic receptor} {alpha-7 nicotinic receptor} {alpha-7 acetylcholine receptor} can bind nicotine and stimulate NMDA receptors [Granon et al., 2003].
If postsynaptic membrane depolarizes and glutamate releases from presynaptic neurons, postsynaptic neuron proteins {NMDA receptor, neuron} {N-methyl-D-aspartate receptor} can bind glutamate [Miller et al., 1989] [Tang et al., 1999] [Watkins and Collingridge, 1989] [Wittenberg and Tsien, 2002]. Binding is fast.
effects
Binding opens sodium ion channels, opens potassium ion channels, opens calcium ion channels, and excites or inhibits. Binding increases cell response non-linearly. Binding rapidly controls connectivity between cells, allowing transient cell assemblies.
In neocortex pyramidal cells, binding causes slow, long lasting ESP that rises to peak in 10 milliseconds to 75 milliseconds and can stay altered for days or years.
process
NMDA receptors have magnesium ion inside. Glutamate binding removes magnesium ion and allows calcium-ion flow. Calcium ion aids protein-kinase phosphorylation. Protein kinases then phosphorylate AMPA receptors for early LTP. Protein kinase A (PKA), MAP kinase (MAPK), and calcium/calmodulin protein kinase (CaMK) phosphorylate CREB. In cell nucleus, CREB activation turns on genes that make late LTP proteins. Active synapses have chemical sites {molecular tag} that bind late LTP proteins.
factors
Brain-derived neurotrophic factor (BDNF) increases NMDA-receptor phosphate binding.
antagonists
Ap5, CGS 19755, CPP, and D-CPP-ene affect NMDA receptor. NMDA antagonists can block visually induced activity in visual-cortex superficial layers, but not deep layers.
Proteins {presynaptic neuroreceptor} can enhance or reduce neurotransmitter release, by responding to previously released neurotransmitter {autoregulation} or to other neurotransmitters or neuromodulators {heteroregulation}. Presynaptic neuroreceptors regulate noradrenaline release from heart, spleen, vas deferens, and brain. Central and peripheral adrenergic-nerve-axon synapses can have both negative and positive feedback.
Proteins {talin} can be for synapse and immune-synapse adhesion.
Proteins {calmodulin protein kinase} {calcium protein kinase} (CaMK) {calcium-calmodulin protein} can phosphorylate, enter cell nucleus, and activate CREB gene.
Proteins {calmodulin-binding protein} can bind to calmodulin and perhaps bind to actin.
At high concentrations, cAMP-dependent protein-kinase catalytic subunits {cAMP-dependent protein kinase} phosphorylate transcription factors, such as cAMP-response element binding protein-1 (CREB-1), C/EBP transcription factor, and tissue plasminogen activator (tPA), which express genes in cell nucleus to initiate change or growth. Repeated action potentials, from stress or high activity, make cAMP-dependent protein kinase concentration high.
Calcium ion entry can activate proteins {cAMP-response element} {cyclic-AMP response element} (CRE) (CRE-1) {cAMP-response element binding protein-1} (CREB-1) {CREB protein} that bind to regulatory regions and activate cyclic-AMP and cyclic-AMP-receptor genes. CREB also activates immediate early genes, such as ubiquitin hydrolase and C/EBP transcription factor, to initiate synaptic growth. CREB regulates endorphin production.
Enzymes {caspase 9} can cause neuron death and so prune networks.
Proteins {C/EBP transcription factor} {C-EBP transcription factor} can activate synaptic protein genes.
Molecules {CREB enhancer} can increase CREB protein by inhibiting phosphodiesterase.
Molecules {CREB suppressor} can decrease CREB protein.
Enzymes {mitogen-activated protein kinase} {MAP kinase} (MAPK) can phosphorylate CREB-2 repressor to prevent CREB-1 binding to CRE-1. MAPK8 regulates cell movement.
Amines {octopamine} can be neuromodulators for behavior.
Enzyme series {phospholipid cascade}| can regulate intracellular phospholipid by regulating gene transcription. Calcium ion, phosphorylation, and phospholipid pathways regulate each other.
Enzyme series {phosphotidylinositol cascade} can regulate intracellular phospholipid by regulating gene transcription.
Enzymes {protein kinase A} (PKA) can phosphorylate and activate mitogen-activated protein kinases.
Proteins {spectrin} {fodrin} can bind to actin and calmodulin.
Proteins {synapsin} can phosphorylate by causing calcium-ion influx.
Proteins {tissue plasminogen activator} (tPA) can activate genes for neuron terminals and spines.
Amines {tyramine} can be neuromodulators for behavior.
Enzymes {tyrosine hydroxylase} (TH) can be rate-limiting enzyme in catecholamine biosynthesis. Increased neuronal firing increases catecholamine-pathway enzyme synthesis in perikarya. Axons transport enzymes to axon terminals. Catecholamine pathway requires pteridine, iron, and oxygen and converts tyrosine to L-DOPA. Dopamine and norepinephrine inhibit tyrosine hydroxylase by feedback inhibition. Stressful stimuli increase TH. Acetylcholine phosphorylates TH using cyclic AMP.
Enzymes {ubiquitin hydrolase} can be in ubiquitin proteasomes, break down PKA regulatory subunit in sense neurons, and so enhance catalysis, typically when cAMP is decreasing.
Proteins {fibronectin} can be in extra-cellular matrix.
Proteins {laminin} can be in extra-cellular matrix.
Proteins {telencephalin} can be cell-adhesion molecules.
Proteins {tubulin} can be in microtubules.
Neurons transfer molecules {neurotransmitter}|.
purposes
Neurotransmitters can transfer signals, mediate rapid electrical communication, foster neuron survival and pathway formation, elicit synaptic changes, and trigger biochemical changes that modify subsequent signals.
types
Transmitter types are amino acidergic, catecholamine, cholinergic, monoaminergic, peptides, and purines. Cholinergic includes acetylcholine. Neurotransmitters include aspartic acid, dopamine, epinephrine, gamma-aminobutyric acid (GABA), glutamic acid, glycine, histamine, norepinephrine, octopamine, and serotonin.
change
Neurotransmitter used by neuron can change over time. Transmitter changes can last days to weeks, while environmental stimuli last seconds to minutes. Neuron can release transmitter at low stimulation, peptide at high stimulation, and both at intermediate stimulation.
vesicles
Cholinergic, monoaminergic, and amino-acidergic neurons synthesize neurotransmitters mostly in nerve terminals. Synaptic vesicles in unmyelinated axon and cell-body regions release neurotransmitters. Released packets have 1000 molecules. Storage vesicles or granules have only one neurotransmitter type. They release independently.
Peptidergic cells synthesize large proteins in cell body and then split them into active peptides.
Individual neurons all have multiple transmitters.
vesicles: dendrites
Mitral cells, substantia nigra dopaminergic neurons, and olfactory bulb GABAergic axonless granule cells have synaptic vesicles in dendrites.
Acetylcholine {acetylcholine, memory} (ACh) can be a fast neurotransmitter or slow modulator.
modulator
ACh regulates neurite nerve process outgrowth and aids neuronal population survival.
location
ACh is in autonomic parasympathetic ganglia, basal forebrain, caudate nucleus, medulla motor nuclei, neuromuscular synapse, Meynart basal nucleus, putamen, pons, superior olive, spinal cord, cranial-nerve motor nuclei, cerebral-cortex bipolar cells, and submandibular-salivary-gland postsynaptic parasympathetic neurons.
excitation
Acute bipolar-cell or parasympathetic-neuron stimulation releases only acetylcholine. Chronic excitation releases both VIP and acetylcholine, in ratio depending on stimulus duration.
VIP
Acetylcholine inhibits VIP release by interacting with neuron receptors. VIP inhibits acetylcholine release by binding to neuron VIP receptors.
drug
Acetylcholine can treat senile dementia or aid memory.
enzyme
Acetylcholinesterase enzyme hydrolyzes acetylcholine. Added cholinesterase decreases memory.
Enzymes {acetylcholinesterase} can hydrolyze acetylcholine. Added cholinesterase decreases memory.
Amino-acid neurotransmitters {amino acidergic neurotransmitters} include glutamate and aspartate.
Amino acids {aspartate} {aspartic acid} can be excitatory transmitters.
Norepinephrine (NE), dopamine (DA), and epinephrine (E) are 3,4-dihydroxy phenylethylamine derivatives {catecholamine}| (CA) {biogenic amine}.
locations
Catecholamines come from tyrosine in peripheral sympathetic neurons, adrenal medulla, chromaffin tissue, and brainstem nuclei.
Adrenal medulla makes and stores catecholamines in response to stress.
metabolism
Catecholamines phosphorylate postsynaptic receptor proteins, like adenylate cyclase, in vascular smooth muscle, heart, liver, adipocytes, and many brain neurons.
Uptake into presynaptic nerve terminal inactivates catecholamines. Desipramine and cocaine inhibit uptake.
Stimulation by serotonin facilitates presynaptic catecholamine release, which increases intraneuronal cAMP, which inactivates potassium-ion channel, which allows more calcium ion in.
Phenylethylamine derivatives release catecholamines. Bretylium and guanethidine have a highly basic center, linked by one-carbon or two-carbon chain to ring, and block catecholamine release.
vesicles
Catecholamines are in membrane-bound vesicles. Reserpine interferes with catecholamine storage in vesicles. Catecholamine release from vesicles uses exocytosis. Release requires calcium ion.
functions
Catecholamines can cause tachycardia, peripheral vasoconstriction, mydriasis, and peristalsis inhibition.
Choline transmitters {cholinergic neurotransmitters} include acetylcholine [Hille, 2001] [Hobson, 1999] [Steriade and McCarley, 1990] [Perry and Young, 2002] [Perry et al., 1999] [Perry et al., 2002] [Woolf, 2002].
Biogenic amines {dopamine}| (DA) are in hypothalamic arcuate nucleus, midbrain nigrostriatal, and ventral midbrain. Dopamine affects reward processing. It initiates and maintains anticipation behavior, novelty, attention, and action selection. Dopamine interacts with amine and choline modulators.
Dopaminergic neurons use adrenaline or epinephrine, noradrenaline or norepinephrine, dopamine, or serotonin. Dopaminergic neurons can make highly branched networks with small-diameter ascending and descending fibers, low frequency potentials, and slow conduction velocities.
Molecules {effector molecule} can work rapidly and break down or reabsorb rapidly.
Fast-acting inhibitory neurotransmitters {gamma-aminobutyric acid} (GABA) can come from glutamate and can be in basal ganglia, cerebellum, cerebral cortex, hippocampus, hypothalamus, retina, striatonigral, thalamus, and ventral pallidum. 20% of inhibitory neurons, mostly interneurons, use GABA. Valium enhances GABA activity.
Fast-acting excitatory amino-acid neurotransmitters {glutamate} {glutamic acid} can be in spinal cord, brainstem, cerebellum, hippocampus, and cerebral cortex. 60% of excitatory neurons, mostly projection neurons, use glutamate. Glutamate affects dopamine.
Amino-acid inhibitory transmitters {glycine} can be in retina and spinal cord.
Amines {histamine, transmitter} can be in pituitary and medial hypothalamus.
Monoamine transmitters {monoaminergic neurotransmitter}| include norepinephrine, epinephrine, dopamine, and serotonin.
Molecules {nitric oxide}| released by postsynaptic terminals can bind to presynaptic terminals. Enzymes {nitric oxide synthase} (NOS) make nitric oxide from arginine. L-nitro-arginine methyl ester (L-NAME) inhibits nitric-oxide synthesis.
Neurotransmitters {peptide neurotransmitter} can have several amino acids.
Spermidine and spermine competitively inhibit amine receptors {polyamine receptor}.
Purine neurotransmitters {purine neurotransmitter}| include AMP and GMP.
Vasoactive monoamines {serotonin}| {5-hydroxytryptamine} (5-HT) can inhibit or excite metabolic activity, depending on receptor. Serotonin comes from tryptophan.
location
Serotonin is in area postrema, medulla oblongata, pineal gland, gut parasympathetic system, and pons raphé nucleus. Brain has 300,000 serotonergic neurons.
functions
Serotonergic-neuron activity is proportional to arousal, wakefulness, and muscular activity. Serotonin excites cortex pyramidal neurons. It inhibits neurons that receive excitations. It regulates neurite nerve process outgrowth and aids neuronal population survival. It causes or inhibits intestinal contraction. It constricts or relaxes blood vessels. Serotonin enhances substance P release from axons to excite spinal cord. Substance P releases serotonin from terminals inhibited by serotonin.
receptors
Neurons make serotonin and release it into synaptic clefts. Mammals have more than 13 different serotonin receptors. Animals have over 30 different serotonin receptors, which connect to G proteins.
uptake
Serotonin reuptake transport molecules remove serotonin from synaptic clefts. Selective serotonin reuptake inhibitors inhibit serotonin uptake back into cells.
damage
If serotonin level decreases, activity increases. Inhibiting serotonin receptor does not modulate behavior.
derivatives
5-HIAA comes from serotonin and causes higher male social status, more female grooming, and quieter activity.
evolution
Serotonergic neurons and serotonin receptors evolved 500,000,000 years ago. Gene duplication allowed different kinds. Anthropoid apes evolved 40,000,000 years ago and have different promoter sequence for serotonin-reuptake-transport gene than humans do.
Molecules {transporter molecule} can put and get transmitters in synaptic cleft. If synapse has no vesicles, it puts transmitters in cleft.
The evidence is against the hypothesis that synapses release neurotransmitter directly {vesigate} from cytoplasm through membrane pores {operator pore} opened by calcium ions.
Sense receptor stimulation can send signal to spinal cord and then to muscle or gland, resulting in involuntary action {reflex, nerve}|. Stimulus can cause innate, immediate response in muscle or gland. Reflex has only one synapse between muscle or tendon touch receptor and motor neurons to muscle. Brain, body, local excitability, and previous reflex responses can affect reflexes.
types
Stretch reflexes relate to muscle tension, posture, and locomotion. Flexion reflexes follow painful skin stimuli. Reflexes {suprasegmental reflex} can be for one vertebra only {segmental reflex} or for all vertebrae above vertebra. Reflexes {intrasegmental reflex} can involve only one spinal segment. Reflexes {intersegmental reflex} can involve several spinal segments. Reflexes can involve spinal cord, cerebellum, and medulla oblongata. Cerebellum and midbrain automatically control muscle movements {synergy, reflex}. Striatum controls muscles automatically and by association. Neocortex exerts voluntary and regulatory control {state variable}.
Thumb pressed into newborn-foot bottom causes foot and toes to flex {ankle clonus}.
Reflexes {arm reflex} can be in newborns.
Scratching a newborn's foot from toe to heel causes big toe to go up and toes to spread {Babiniski reflex}. In infants, stroking foot side causes big-toe raising. Babiniski reflex disappears at eighteen months old. Adult apes have Babiniski reflex, to grasp tree branches with toes.
Baby reacts to red rattle {Brazelton sensory test}. Baby eyes look ahead during spinning and return to center when spinning stops. Baby can hear bell ring with both ears.
If small object irritates eye, eyelid reflexively closes {blink reflex}.
Reflexes {crossed extension reflex} can be suprasegmental and happen after flexion.
Insects and vertebrates have fast reflexes {escape reflex} to leave situation.
Reflexes {eye reflex} can be in newborns.
Reflexes {eyelid closing reflex} can be in newborns.
Pain causes muscle flexion {flexion reflex}.
Reflexes {inverse stretch reflex} {inverse myotactic reflex} {Golgi tendon reflex} {clasp-knife reflex} can override stretch reflex but is slower because it has two synapses. It works with stretch reflex to maintain posture.
Touching male inner thigh can cause penis erection and testes raising {inner thigh reflex}.
Tapping newborn chin causes masseter muscle to contract {jaw-jerk}.
Avoiding or fleeing is a reflex {large moving object reflex} to large moving objects.
Newborns can react to head-position fast change by extending arms and fingers to side and then in front {Moro reflex}. Moro reflex lasts until six months old.
A one-synapse reflex {stretch reflex} {myotactic reflex} maintains posture and muscle tone. Stretch reflexes relate to muscle tension, posture, and locomotion. Stretch reflexes maintain posture by contracting muscles if they stretch out. Stretch reflex control allows sitting up and other behaviors, after sense organs establish reflexes with motor neurons. Standing, crawling, sitting, walking, and running use spinal-cord reflex circuits, which connect to cerebrum and cerebellum.
Reflexes {necking reflex} can be in newborns.
New stimulus causes attention and turning toward stimulus {orientation reflex} {orienting response}, with increased brain electrical activity, reduced blood flow to extremities, changed skin electrical resistance, increased adrenal steroid hormones, and overt motor activity. Behavior interruption, perception discrepancy, or unexpected stimuli can cause animals to turn toward changes, have more sensitization, and concentrate more. Orienting reflex is automatic and involuntary, not cognitive. It involves acetylcholine neurons. It precedes attention. It processes up to 2000 information bits [Koffka, 1935] [Köhler, 1969] [Palmer, 1999].
ACTH prolongs orientation reflex, and glucocorticoids dull it.
orientation sense
Orienting response precedes slower process {orientation sense} that gathers information about time, place, and person to recognize object. Orientations {shifter circuit, orientation} can be automatic but voluntary and cognitive. Circuits process 50 information bits with each glimpse. Orientation places objects in scenes in short-term memory {pop-out, orientation}, using motion, depth, texture, and color cues.
Eye pupil can open {pupil dilation reflex}|.
Reflexes {pupillary reflex} can be in newborns.
Newborns have reach-and-grasp reflex arm and hand movement {reach-and-grasp reflex}.
Animals can make themselves upright reflexively {righting reflex}.
Touching mouth corner causes newborns to turn and try to suck {rooting response}.
Stimulating a skin point makes same-side leg scratch that point {scratch reflex}. Scratch reflex is suprasegmental.
Jawed vertebrates snap at food {snapping at food reflex}, if small objects move in vision field.
Fear increases startle response {fear-potentiated startle response} {startle response, reflex} {startle reflex}.
Cerebellum and midbrain can coordinate muscle movements {synergy, movement}.
A tendon tap can cause muscle contraction {tendon jerk}. Tendon jerk is simplest and fastest mammalian reflex.
Newborn resists being pulled into sitting position {traction reflex}.
Newborns turn in direction of voices from behind curtains, moving both hands and face {voice reflex}.
After sticking pin into foot sole, newborn foot and leg withdraw {withdrawal reflex}.
Sense-organ neurons {afferent nerve} {afferent fiber} send to ganglia outside brain along spinal cord. Ganglia sense neurons send one axon to brain and one axon to peripheral nerve.
Axons to brain synapse on brain secondary sense neurons. Secondary sense neurons send to cerebellum or thalamus. Thalamus neurons send to neocortex. Neocortex neurons send back to thalamus and to cortex association areas. Association cortex neurons send to hippocampus and amygdala. Hippocampus and amygdala neurons send to hypothalamus.
All these cortical regions send to corpus striatum. Corpus striatum neurons send to globus pallidus. Globus pallidus neurons send to reticular formation and thalamus.
muscle
Muscle sense-cell afferent is wide axon and has one synapse, because large axons have lower thresholds.
skin
Skin afferent is fine axon with several synapses, because fine axons have higher thresholds.
Brain neurons {efferent nerve} {efferent fiber} send to sense organs, muscles, and glands.
Large myelinated axons {A fiber} can come from motor or sense neurons. A fibers {A-alpha nerve} {alpha fiber} can be for proprioception or be somatic motor axons. Sensory A fibers {A-beta nerve} {beta fiber} can be for touch or pressure and travel in spinal cord from trigeminal nucleus. Intermediate-size myelinated sensory A fibers {A-delta nerve} {delta fiber} can be for pain, temperature, or touch and travel in spinal cord to trigeminal nucleus. Motor A fibers {A-gamma fiber} {gamma fiber} can be for muscle spindles.
Small myelinated axons {B fiber} are preganglion autonomic nerves.
Small unmyelinated axons {C nerve} {C fiber} are postganglion sympathetic autonomic nerves or are dorsal root nerves for pain, temperature, and reflexes. Unmyelinated sense-nerve axons travel from spinal cord dorsal roots to trigeminal nucleus. Unmyelinated axons have few branches.
Dopamine-secreting neurons {dopamine neuron} are for goals.
Sensory axons {Ia fiber} can be for muscle spindle and annulospiral endings.
Sensory axons {Ib fiber} can be for Golgi tendon organ.
Sensory axons {II fiber} can be for muscle spindle, flower spray ending, touch, or pressure.
Sensory axons {III fiber} can be for pain, temperature, and touch.
Neurons {interneuron}| can connect across two nerve pathways. After pathway neuron excites them, interneurons typically inhibit or excite other-pathway neurons. Interneurons can detect correlations among local neuron signals. They note constancies and covariances between pathways. Symmetric connections coordinate pathway neurons in ganglia and cortex, especially in topographical maps. Asymmetric inhibitory connections among neurons and interneurons allow associative learning. Interneurons arose from neuron duplication.
Sensory axons {IV fiber} can be for pain or other receptors.
Fruitfly brain cells {Kenyon cell} receive from electric-shock dopamine cells and from odor cells and possibly send to motor neurons.
Unmyelinated C fibers and slightly myelinated A-delta fibers {nociceptive fiber} go to trigeminal nucleus for noxious stimuli, pain, or punishment.
Medulla respiratory center sends excitatory signals along nerve {phrenic nerve} to diaphragm.
Legs have a main nerve {sciatic nerve}|.
Body neurons {somatic neuron} can connect to striated muscles to perform voluntary actions and can be active or quiet, depending on will.
Spinal cord nerves {spinal nerve} are two per vertebra and include dorsal nerves, ventral nerves, and visceral autonomic nerves.
Spinal nerves include visceral branches {autonomic nerve}.
Spinal nerves can be on back {dorsal nerve}.
Spinal nerves can be on side and front {ventral nerve}.
Head has cranial nerves 1 through 12 {cranial nerve}.
Cranial nerve 1 {olfactory nerve} {cranial nerve 1} {cranial nerve I} has axons from nose olfactory-sense neurons, through cribriform plate, to olfactory bulb. Vertebrate smell uses first cranial nerve.
Cranial nerve 2 {optic nerve} {cranial nerve 2} {cranial nerve II} is from retina to thalamus. It leaves the retina at a location with no receptors {optic disk}.
Cranial nerve 3 {oculomotor nerve} {cranial nerve 3} {cranial nerve III} sends to extrinsic eye muscles, upper eyelid elevator muscle, ciliary muscle, and pupil sphincter muscle. Extrinsic eye muscles are inferior oblique, superior rectus, inferior rectus, and medial rectus, but not lateral rectus or superior oblique.
Cranial nerve 4 {trochlear nerve} {cranial nerve 4} {cranial nerve IV} sends to superior oblique eye muscles.
Cranial nerve 5 {trigeminal nerve} {cranial nerve 5} {cranial nerve V} is from face and carries smell coolness or hotness.
Cranial nerve 6 {abducens nerve} {cranial nerve 6} {cranial nerve VI} sends to lateral rectus eye muscles.
Cranial nerve 7 {facial nerve} {cranial nerve 7} {cranial nerve VII} is from face and has branch {chorda tympani nerve} from anterior mobile tongue that travels with trigeminal-nerve lingual branch as it leaves tongue, goes to middle ear, goes to brain, and signals taste.
Cranial nerve 8 {auditory nerve} {vestibulocochlear nerve} {cranial nerve 8} {cranial nerve VIII} is from inner ear and has cochlear-nerve axons, from hair cells to brain, and vestibular-nerve axons, from vestibule to brain.
Cranial nerve 9 {glossopharyngeal nerve} {cranial nerve 9} {cranial nerve IX} is from pharynx and controls swallowing, tasting, and saliva release.
Cranial nerve 10 {vagus nerve, cranial nerve}| {cranial nerve 10} {cranial nerve X} goes from heart, lungs, stomach, intestine, larynx, esophagus, and aorta to nucleus tractus solitarius. It connects brain to lungs, heart, and intestines.
Cranial nerve 11 {spinal accessory nerve} {cranial nerve 11} {cranial nerve XI} is from shoulder.
Cranial nerve 12 {hypoglossal nerve} {cranial nerve 12} {cranial nerve XII} is from tongue.
Cells {glia}| can provide neuron covering and environment.
covering
Glia cover nerve surfaces, except at synapses and nodes of Ranvier.
structure
Glia provide paths for migrating neurons.
properties
Glia are contractile. Glia can divide. Glia do not conduct. Glia do not interact electrically with neurons. Perhaps, glia are polarizable [Cornell-Bell et al., 1990] [Laming et al., 1998] [Sanderson, 1996].
types
Oligodendrocytes and astrocytes are macroglia. Macrophages are microglia.
chemicals
Glia make myelin, which surrounds axons. Glia make amino acids for neurons. Glia maintain extracellular fluid chemical concentrations. Glia have cholinesterase, whereas neurons have acetylcholinesterase. Glia have much less RNA than neurons.
chemicals: synapses
Glia respond to ATP that leaves synapses by letting calcium in and changing proteins made. Astrocytes make thrombospondin, which builds synapses.
chemicals: regulation
Glia and neuron membranes, receptors, and chemicals interact. Glia regulate extracellular ion, neurotransmitter, and other small-molecule concentrations. Glia can release reactive oxygen molecules, nitric oxide, prostaglandins, excitatory amino acids, IL-1, and nerve growth factor. Excitatory amino acids are N-methyl-D-aspartate and non-NMDA agonists. These can excite pain-responsive spinal cord neurons and increase neurotransmitter release from nerves that relay pain information to spinal cord.
chemicals: factors
Substances released by neurons affect glia [Araque et al., 1999] [DeLeo and Yezierski, 2001] [Raghavendra and DeLeo, 2003] [Watkins et al., 2001].
numbers
Human brains have nine glial cells for every neuron. Glia-to-neuron ratio is as much as 20-to-1 in humans. Glia are half of brain mass. Rats have four or five glial cells for each neuron. The higher human glia-to-neuron ratio reflects need for more chemical and electrical environments and neural connections [Araque et al., 1999] [DeLeo and Yezierski, 2001] [Raghavendra and DeLeo, 2003] [Watkins et al., 2001].
Macroglia {astrocyte} can be protoplasmic, with branched processes, or fibrous, not branched. They cover blood vessels, neurons, and external brain surfaces. They provide structure and guides neuron migration. They take up potassium ions and neurotransmitters. Some astrocytes repair nervous tissue. Astrocytes affect metabolic disorders and epilepsy.
Glia membranes {blood-brain barrier}| (BBB) {glial membrane} can surround nervous-system blood vessels, delay sodium and potassium ion passage, and block passage of other ions and molecules. BBB is interface between blood capillaries and brain tissue.
Glia connect by gap junctions {gap junction, glia}. Electrical stimulation can spread rapidly through connected glia [Araque et al., 1999] [DeLeo and Yezierski, 2001] [Raghavendra and DeLeo, 2003] [Watkins et al., 2001].
oligodendrocytes or astrocytes {macroglia}.
Central nervous system macrophages {microglia} absorb and digest dead cells. They also receive signals from immune cells. They can react to pathogens. Perhaps, they can receive signals from viruses and damaged nerves. They do not affect normal pain responses but can cause abnormally high pain when they receive signals from immune cells [Kreutzberg, 1996] [Meller et al., 1994] [Watkins et al., 2001]. Astrocytes become active when microglia become active.
Microglia make surface receptors {microglia receptor} for macrophage antigen complex-1 (Mac-1), phagocytosis, and cytotoxic-molecule production, including reactive oxygen molecules, nitric oxide, prostaglandins, and proinflammatory cytokines such as interleukin (IL) and tumor necrosis factor (TNF) [Hopkins and Rothwell, 1995].
Macroglia {oligodendrocyte} makes myelin and wraps from several to 50 axons. Oligodendrocytes affect multiple sclerosis and spinal cord injury.
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Date Modified: 2022.0225