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 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.
Detection of noxious stimuli
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 dorsal root ganglia. Others are specialised structures in the skin such as nociceptive Schwann cells. 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 fibers that normally carry non-noxious stimuli to be perceived as noxious. Nociceptive pain consists of an adaptive alarm system. 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 neuron's axon 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 periods of effect. After establishing a baseline, the drug under test is given, and the elevation in threshold is recorded at specified times. The threshold should return to the baseline (pretreatment) value when the drug wears off. In some conditions, the excitation of pain fibers increases as the pain stimulus continues, leading to a condition called hyperalgesia.
Theory
Consequences Nociception can also cause generalized autonomic responses before or without reaching consciousness to cause pallor, sweating, tachycardia, hypertension, lightheadedness, nausea, and fainting.
System overview
This overview discusses proprioception, thermoception, chemoception, and nociception, as they are all integrally connected.
Mechanical
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. 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 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. 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.
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