The pain system has skin receptors with ion channels, neurons, fibers, fiber tracts, and brain regions. Pain chemical receptors send to dorsal-horn neurons, which send to cortical regions. Cortex and thalamus control pain {pain, anatomy}.
Skin and body receptors (nociceptor) chemically bind endomorphins, prostaglandins, bradykinin peptides, and protein hormones (such as nerve growth factor), molecules released by inflammation and tissue damage [Woolf and Salter, 2000].
fibers
Body organs and mesentery have pain fibers. Internuncial neurons have pain fibers. Pain fibers are A, C, III, IV, and nociceptive fibers. Large myelinated fibers detect moderate stimulation. Small myelinated fibers detect all stimulations. Myelinated fibers detect sharp localized skin pain. Unmyelinated fibers detect dull deep unlocalized body pain. Itching nerves are separate from pain nerves.
brain
Anterior cingulate gyrus, frontal lobe, Lissauer's tract, locus coeruleus, nociceptive system, protopathic pathway, raphé nuclei, reticular formation, sensory reticular formation, sensory thalamus, spinal cord, spinoreticular tract, and spinothalamic tract affect pain. Throbbing pain, burning pain, and sharp pain use different brain regions. Cingulate cortex receives pain information [Chapman and Nakamura, 1999]. Cortex has pain center connected to sense areas. Reticular formation regulates pain.
brain pathways
Feeling pain and reacting to it involve separate pathways. Spinothalamic tract and central gray-matter path carry pain fibers. Internuncial neurons have pain fibers. Body organs and mesentery have pain fibers. Lemniscal tract has no pain fibers but affects pain. Abdominal pain signals travel in subdiaphragmatic vagus nerve to nucleus tractus solitarius, nucleus raphe magnus, and spinal-cord dorsolateral funiculus [Ritter et al., 1992].
Connective-tissue dendritic cells {nerve-associated lymphoid cells} (NALC) have interleukin-1 binding sites, send to sensory vagus-nerve paraganglia, and are near macrophages, mast cells, and other dendritic cells [Goehler et al., 1999].
Connective-tissue nerve-associated lymphoid cells send to neuron groups {paraganglia} who send along sensory vagus nerve [Goehler et al., 1999].
Nociceptors can have proton ion channels {acid-sensing ion channel} (ASIC).
Nociceptors and other neurons have special calcium-ion channels {N-type calcium channel} {calcium channel, N-type}. Ziconotide (Prialt), modified cone-snail venom, inhibits N-type calcium channels to lessen pain. Gabapentin (Neurontin) anticonvulsant binds to N-type calcium channels.
Outside CNS, nociceptors and other neurons have special sodium-ion channels {TTX-resistant voltage-gated sodium channel}.
Nociceptors and all neurons have sodium-ion channels {voltage-gated sodium channel} {sodium channel, voltage-gated} that open by voltage changes.
Nociceptors can have receptors {bradykinin receptor} for small bradykinin peptides, produced by peripheral inflammation.
Dorsal-horn neurons receive input from nociceptors and have calcitonin peptide receptors {calcitonin receptor} {calcitonin gene-related peptide receptor} (CGRP receptor).
Mouth nociceptors can have pepper-molecule receptors {capsaicin receptor} {VR1 receptor}, which also react to high temperature and protons.
Peripheral pain nerves can add chemical receptors {hormone receptor}. For example, stress hormones can attach to stress-hormone receptors and cause pain [Woolf and Salter, 2000].
Nociceptors can have protein-hormone receptors {nerve growth factor receptor} (NGF receptor).
All neurons that receive input from nociceptors have glutamate receptors {NMDA receptor, pain}. Dorsal-horn neurons have glutamate receptors with a specific subunit {NR2B subunit}.
NTRK1 gene makes receptors {neurotrophin tyrosine kinase receptor type 1} (NTRK1 receptor). NTRK1-gene mutations can cause a rare autosomal recessive disease (CIPA), with pain insensitivity, no sweating, self-mutilation, fever, and mental retardation.
Skin receptors {nociceptor} can detect pain, to warn about skin damage.
Many neurons, including nociceptors, have opium-compound receptors {opioid receptor}.
Nociceptors can have endomorphin receptors {prostaglandin receptor}.
Dorsal-horn neurons receive input from nociceptors and have substance-P receptors {neurokinin-1 receptor} (NK-1 receptor) {substance P receptor}. Substance P can carry saporin toxin into dorsal-horn neurons and kill them.
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Date Modified: 2022.0225