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}.
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Date Modified: 2022.0225