利用者:加藤勝憲/侵害受容
侵害受容(nociception、/ˌnəʊɪˈɛ pʃ(ə)n/)とは、侵害刺激を符号化する感覚神経系のプロセスのことである。これは、生物が痛みを伴う刺激を受け、それを分子シグナルに変換し、適切な防御反応を引き起こすためにシグナルを認識し特徴付けるために必要な一連の出来事とプロセスを扱う。
In physiology, nociception (/ˌnəʊsɪˈsɛpʃ(ə)n/), also nocioception; 言語は ラテン語 nocereで意味は'to harm/hurt') is the sensory nervous system's process of encoding noxious stimuli. It deals with a series of events and processes required for an organism to receive a painful stimulus, convert it to a molecular signal, and recognize and characterize the signal to trigger an appropriate defensive response.
侵害受容では、侵害受容器と呼ばれる感覚ニューロン への激しい化学的(例:唐辛子やカイエンペッパーに 含まれるカプサイシン)、機械的(例:切る、つぶす)、熱 的(熱や冷)刺激が、神経線維の連鎖に沿って脊髄を 介して脳へと伝わる[1]、 侵害受容は、攻撃から生体を守るための様々な生理的・行動的反応を引き起こし、通常、感覚を持つ生物において痛みの主観的経験、すなわち知覚をもたらす[2]。
In nociception, intense chemical (e.g., capsaicin present in chili pepper or cayenne pepper), mechanical (e.g., cutting, crushing), or thermal (heat and cold) stimulation of sensory neurons called nociceptors produces a signal that travels along a chain of nerve fibers via the spinal cord to the brain. Nociception triggers a variety of physiological and behavioral responses to protect the organism against an aggression, and usually results in a subjective experience, or perception, of pain in sentient beings.
侵害刺激の検出
[編集]機械的、熱的、化学的刺激は、侵害受容器と呼ばれる神経終末によって感知される。侵害受容器は、皮膚、骨膜などの体表面、関節表面、一部の内臓に存在する。
侵害受容器は、皮膚、骨膜などの内部表面、関節表面、 およびいくつかの内臓に存在する。侵害受容器は、受容器から脊髄や脳へ向かう軸索によって分類される。神経損傷後、通常は非侵害性刺激を伝える触覚線維が、侵害性刺激として知覚されることがある。
一部の侵害受容器は、脊髄の外側の背側根神経節に細胞体を持つ、特殊化されていない自由神経終末である[3]。 その他は、侵害受容性シュワン細胞のような、皮膚の特殊化された構造体である[4]。侵害受容器は、受容体から脊髄または脳に伝わる軸索に従って分類される。 神経損傷後は、通常は非有害な刺激を伝える接触線維が有害であると認識される可能性がある。[5]
Potentially damaging mechanical, thermal, and chemical stimuli are detected by nerve endings called nociceptors, which are found in the skin, on internal surfaces such as the periosteum, joint surfaces, and in some internal organs. Some nociceptors are unspecialized free nerve endings that have their cell bodies outside the spinal column in the dorsal-root ganglia.[3] Others are specialised structures in the skin such as nociceptive schwann cells.[4] Nociceptors are categorized according to the axons which travel from the receptors to the spinal cord or brain. After nerve injury it is possible for touch fibres that normally carry non-noxious stimuli to be perceived as noxious.[5]
Nociceptive pain consists of an adaptive alarm system.[6] Nociceptors have a certain threshold; that is, they require a minimum intensity of stimulation before they trigger a signal. Once this threshold is reached, a signal is passed along the axon of the neuron into the spinal cord.
侵害受容性痛覚は、適応的なアラームシステムで構成さ れている。侵害受容器には一定の閾値があり、すなわち、 信号を発する前に最小強度の刺激が必要である。この閾値に達すると、信号はニューロンの軸索に沿っ て脊髄に伝達される。
侵害受容閾値検査では、人間または動物の被験者に意図的に有害な刺激を加えて痛みを研究する。
動物では、この技術は鎮痛薬の有効性を研究し、投与量と効果の期間を確立するためによく使用される。 ベースラインを確立した後、試験対象の薬剤が投与され、指定された時間に閾値の上昇が記録される。 薬の効果がなくなると、閾値はベースライン (治療前) の値に戻るはずである。 状況によっては、痛みの刺激が続くと痛み線維の興奮が大きくなり、痛覚過敏と呼ばれる状態が引き起こされる。
Theory
[編集]Template:Sensation and perception
Consequences
[編集]Nociception can also cause generalized autonomic responses before or without reaching consciousness to cause pallor, sweating, tachycardia, hypertension, lightheadedness, nausea, and fainting.[7]
System overview
[編集]This overview discusses proprioception, thermoception, chemoception, and nociception, as they are all integrally connected.
Mechanical
[編集]Proprioception is determined by using standard mechanoreceptors (especially ruffini corpuscles (stretch) and transient receptor potential channels (TRP channels). Proprioception is completely covered within the somatosensory system, as the brain processes them together.
Thermoception refers to stimuli of moderate temperatures 24–28 °C (75–82 °F), as anything beyond that range is considered pain and moderated by nociceptors. TRP and potassium channels [TRPM (1-8), TRPV (1-6), TRAAK, and TREK] each respond to different temperatures (among other stimuli), which create action potentials in nerves that join the mechano (touch) system in the posterolateral tract. Thermoception, like proprioception, is then covered by the somatosensory system.[8][9][10][11][12]
TRP channels that detect noxious stimuli (mechanical, thermal, and chemical pain) relay that information to nociceptors that generate an action potential. Mechanical TRP channels react to depression of their cells (like touch), thermal TRPs change shape in different temperatures, and chemical TRPs act like taste buds, signalling if their receptors bond to certain elements/chemicals.
Neural
[編集]- Laminae 3-5 make up nucleus proprius in spinal grey matter.
- Lamina 2 makes up substantia gelatinosa of Rolando, unmyelinated spinal grey matter. Substantia receives input from nucleus proprius and conveys intense, poorly localized pain.
- Lamina 1 primarily project to the parabrachial area and periaqueductal grey, which begins the suppression of pain via neural and hormonal inhibition. Lamina 1 receive input from thermoreceptors via the posterolateral tract. Marginal nucleus of the spinal cord are the only unsuppressible pain signals.
- The parabrachial area integrates taste and pain info, then relays it. Parabrachial checks if the pain is being received in normal temperatures and if the gustatory system is active; if both are so the pain is assumed to be due to poison.
- Ao fibers synapse on laminae 1 and 5 while Ab synapses on 1, 3, 5, and C. C fibers exclusively synapse on lamina 2.[13][14]
- The amygdala and hippocampus create and encode the memory and emotion due to pain stimuli.
- The hypothalamus signals for the release of hormones that make pain suppression more effective; some of these are sex hormones.
- Periaqueductal grey (with hypothalamic hormone aid) hormonally signals reticular formation's raphe nuclei to produce serotonin that inhibits laminae pain nuclei.[15]
- Lateral spinothalamic tract aids in localization of pain.
- Spinoreticular and spinotectal tracts are merely relay tracts to the thalamus that aid in the perception of pain and alertness towards it. Fibers cross over (left becomes right) via the spinal anterior white commissure.
- Lateral lemniscus is the first point of integration of sound and pain information.[16]
- Inferior colliculus (IC) aids in sound orienting to pain stimuli.[17]
- Superior colliculus receives IC's input, integrates visual orienting info, and uses the balance topographical map to orient the body to the pain stimuli.[18][19]
- Inferior cerebellar peduncle integrates proprioceptive info and outputs to the vestibulocerebellum. The peduncle is not part of the lateral-spinothalamic-tract-pathway; the medulla receives the info and passes it onto the peduncle from elsewhere (see somatosensory system).
- The thalamus is where pain is thought to be brought into perception; it also aids in pain suppression and modulation, acting like a bouncer, allowing certain intensities through to the cerebrum and rejecting others.[20]
- The somatosensory cortex decodes nociceptor info to determine the exact location of pain and is where proprioception is brought into consciousness; inferior cerebellar peduncle is all unconscious proprioception.
- Insula judges the intensity of the pain and provides the ability to imagine pain.[21][22]
- Cingulate cortex is presumed to be the memory hub for pain.[23]
Nociception has been documented in other animals, including fish[24] and a wide range of invertebrates,[25] including leeches,[26] nematode worms,[27] sea slugs,[28] and fruit flies.[29] As in mammals, nociceptive neurons in these species are typically characterized by responding preferentially to high temperature (40 °C or more), low pH, capsaicin, and tissue damage.
History of term
[編集]The term "nociception" was coined by Charles Scott Sherrington to distinguish the physiological process (nervous activity) from pain (a subjective experience).[30] It is derived from the Latin verb nocēre, which means "to harm".
See also
[編集]References
[編集][[Category:感覚系]] [[Category:疼痛]] [[Category:未査読の翻訳があるページ]]
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