The receptors that perceive pain stimuli (nociceptors) are thin branches of sensory fibers - free nerve endings that are found in abundance in the skin and other tissues, according to Pannochka, an Internet publication for girls and women from 14 to 35 years old.. net In addition, in the skin and especially in the dentin of the teeth, peculiar complexes of free nerve endings with cells of the innervated tissue were found, which are considered as complex receptors for pain sensitivity (Matthews B. , 1985).

Pain receptors are shared by:.

1) by belonging to the innervated tissue (located in various layers of the skin, subcutaneous base, mucous membranes, periosteum, muscles, organs of the chest and abdominal cavities);

2) by belonging to the type of sensitive neurons.

The first type of nociceptors is anatomically represented by free nerve endings branched in the form of a tree (thin myelin fibers). They are fast A-delta fibers that conduct irritation at a speed of 6-30 m / s. These fibers are excited by high-intensity mechanical (pinprick) and sometimes thermal skin irritation.. A-delta nociceptors are located primarily in the skin and joints. A-delta fiber transmitter remains unknown.

Another type of nociceptor is represented by dense unencapsulated glomerular bodies (nonmyelinated C-fibers), conducting stimulation at a speed of 0.5-2 m / s. These afferent fibers in humans and other primates are represented by polymodal nociceptors, therefore they react to both mechanical and thermal and chemical stimuli..

They are activated by chemicals arising from tissue damage, being at the same time chemoreceptors. C-fibers are distributed throughout all tissues with the exception of the central nervous system. However, they are also present in peripheral nerves as nervi nervorum. Fibers that have receptors that sense tissue damage contain substance P, which acts as a transmitter.

This type of nociceptor also contains the calcitonin-gene-binding peptide, and fibers from the viscera contain a vasoactive intestinal peptide (Nicholls et al.. , 1992);

3) by the origin of the pain stimulus - mechanical, thermal, etc..

4) according to the ability to be activated by painful stimuli of various origins: monomodal - reacting only to one type of nociceptive stimulus (mechanical, thermal, etc.. polymodal - responding simultaneously to nociceptive stimuli of various origins;

5) according to the quality of pain that occurs in a person - receptors for acute localized pain and dull diffuse pain.

The discovery of opioid peptides and receptors dating back to the early 70s led to the formation of a new view of the pathophysiological processes of the development and relief of pain. In 1973, Kosterlitz and Yaksh identified the sites of morphine application, and two years later the localization of natural peptides that mimic the action of morphine was discovered..

Three classes of opioid receptors are of clinical importance: ?, kappa and delta receptors (Kosterlitz, Paterson, 1985). Their distribution within the CNS is highly variable.. Dense placement of receptors found in the posterior horns of the spinal cord, in the midbrain and thalamus. Immunocytochemical studies have shown that the highest concentration of spinal opioid receptors is located in the superficial layers of the posterior horns of the spinal cord..

Endogenous opioid peptides (enkepapine, eidorphin, dynorphin) are released and interact with opioid receptors whenever pain stimulation occurs as a result of overcoming the pain threshold. The fact that many opioid receptors are located in the surface layers of the spinal cord means that opiates can easily enter it from the surrounding cerebrospinal fluid.. Experimental observations (Yaksh, Rudy, 1976) of the direct spinal action of opiates led to the possibility of their therapeutic use by intrathecal (Wang, 1977) and epidural (Bromage et al.. , 1980) introduction.

What are the pathophysiological mechanisms of pain impulse transmission Tissue damage causes depolarization of nerve endings (nociceptors), leading to their excitation, and this process spreads along the afferent fiber in the form of electrical signals - action potentials that reach the spinal cord. Discharges of primary afferent fibers at the site of tissue damage cause the release of vesicles in axons containing substance P type neuropeptides, which sensitize nociceptors and increase their frequency of discharges.

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