The neurochemical mechanisms of pain

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The functional activity of the neurophysiological mechanisms of pain sensitivity system implemented neurochemical processes at various levels of nociceptive and antinociceptive systems.

Peripheral nociceptors are activated under the influence of many of the endogenous biologically active substances -. Histamine, substance P, kinins, prostaglandins, etc. An important role in the field in primary nociceptive neurons plays substance P. It is considered as a mediator of pain. Capsaicin (a substance found in red pepper) is a violation of substance P synthesis; intrathecal administration of capsaicin in the region of the spinal cord is a long analgesia; with the effect of capsaicin could be linked to the analgesic effect of pepper patch. At the higher levels of the nociceptive system also has a substance P, but holding them in excitation is carried out mainly by the neurotransmitters, which are inherent in the neurons of these levels. In the processes of excitation in different parts of the nociceptive system involving various neuropeptides, which, as in other parts of the central nervous system, act as neuromodulators.

The neurochemical mechanisms of activity of endogenous antinociceptive system implemented neuropeptides and neurotransmitters classic. Analgesia is caused, as a rule, the combined or sequential action of several transmitters.

Effective endogenous opioid analgesics are neuropeptides (the enkephalins, endorphins). They depressing effect on transmission neurons and activating it - on neurons antinociceptive system, stimulate the system of diffuse nociceptive inhibitory control (DNIC), change the activity of neurons in the higher parts of the brain that perceive nociceptive stimulation and involved in the formation of painful sensations. Their effects are also realized through the action of serotonin, norepinephrine, and other neurotransmitters. Also induce analgesia and other neuropeptides (neurotensin, cholecystokinin, bombesin, angiotensin, vasopressin and others.). Substance P may also cause analgesia and inhibition of pathological pain, even when it is in the antinociceptive action of the structure, such as the dorsal nucleus of the seam.

From classical neurotransmitters important role in the analgesic effects play serotonin, norepinephrine, dopamine, GABA. Serotonin is a neurotransmitter antinociceptive systems at the spinal level. However, one of the parts of the serotoninergic system activity participates in nociceptive system, it enhances the sensitivity of nociceptive field.

Norepinephrine is also the mediator of the descending antinociceptive system, it inhibits the activity of nociceptive neurons in the posterior horns of the spinal cord and the nuclei of the trigeminal nerve. Furthermore, norepinephrine suppresses pain mechanisms and at the supraspinal level. Its analgesic effect is associated with the activation of α-adrenergic receptors, as well as involving the serotoninergic system. Therefore, an activator of the central α-adrenergic clonidine causes a pronounced analgesic effect.

GABA is involved in the suppression of activity of nociceptive neurons and pain at the spinal level. Violation of GABAergic inhibitory processes (for example, by exposing the posterior horns of tetanus toxin, penicillin, and others.) Causes the formation therein generator and heavy pain of spinal origin. In the middle and medulla can inhibit GABA neurons antinociceptive structures and weaken the mechanisms of pain relief at this level.