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Nociception

(Redirected from Pain receptors)

In physiology, nociception (/ˌnəʊsɪˈsɛpʃ(ə)n/), also nocioception; from Latin nocere '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.

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.[1] 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.[2]

Detection of noxious stimuli

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Mechanism of nociception via sensory afferents

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.

Nociceptive threshold testing deliberately applies a noxious stimulus to a human or animal subject to study pain. In animals, the technique is often used to study the efficacy of analgesic drugs and to establish dosing levels and period of effect. After establishing a baseline, the drug under test is given and the elevation in threshold recorded at specified times. When the drug wears off, the threshold should return to the baseline (pretreatment) value. In some conditions, excitation of pain fibers becomes greater as the pain stimulus continues, leading to a condition called hyperalgesia.

Theory

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Main article: Pain theories

Consequences

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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

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This diagram linearly (unless otherwise mentioned) tracks the projections of all known structures that allow for pain, proprioception, thermoception, and chemoception to their relevant endpoints in the human brain. Click to enlarge.

This overview discusses proprioception, thermoception, chemoception, and nociception, as they are all integrally connected.

Mechanical

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See also: Neuropathic pain

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

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In non-mammals

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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

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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

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  • Electroreception – Biological electricity-related abilities
  • Mechanoreceptor – Sensory receptor cell responding to mechanical pressure or strain
  • Thermoception – Sensation and perception of temperature
  • Proprioception – Sense of self-movement, force, and body position

References

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  29. ^ Tracey, W.Daniel; Wilson, Rachel I; Laurent, Gilles; Benzer, Seymour (April 2003). "painless, a Drosophila Gene Essential for Nociception". Cell. 113 (2): 261–273. doi:10.1016/s0092-8674(03)00272-1. PMID 12705873. S2CID 1424315.
  30. ^ Sherrington, C. (1906). The Integrative Action of the Nervous System. Oxford: Oxford University Press.[page needed]
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