Kipureseptorit

Kipureseptorit, or pain receptors, are specialized free nerve endings that detect stimuli indicating potential or actual tissue damage. They are part of the peripheral nervous system and arise from small-diameter primary afferent neurons whose cell bodies reside in the dorsal root ganglia or the trigeminal ganglion. Kipureseptorit are distributed in skin, mucous membranes, muscles, joints, and some visceral tissues, forming the initial detectors of noxious stimuli.

Most kipureseptorit are divided into modalities based on their activating stimuli: mechanical, thermal, chemical, or polymodal. Mechanical nociceptors respond to damaging pressure or stretch; thermal nociceptors detect extreme temperatures; chemical nociceptors respond to irritants and inflammatory mediators; polymodal nociceptors can be activated by more than one type of noxious stimulus. The transduction of these stimuli involves a variety of ion channels and receptors expressed on the free nerve endings.

Key molecular players include TRPV1 (heat and chemical irritants such as capsaicin), TRPA1, various acid-sensing and purinergic receptors, and mechanosensitive channels like PIEZO2. Following activation, kipureseptorit generate action potentials that propagate along Aδ fibers (rapid, sharp pain) or C fibers (dull, lingering pain) to the dorsal horn of the spinal cord or the equivalent brainstem nuclei in the head. There, they release neurotransmitters such as glutamate and neuropeptides (e.g., substance P, CGRP), contributing to pain perception and reflex withdrawal.

Peripheral and central sensitization can lower pain thresholds after tissue injury and inflammation, amplifying nociceptive signaling. Kipureseptorit are central to both protective reflexes and the experience of pain, and they remain a major target for analgesic strategies and research.