Subpopulations of “nocifensor neurons” contributing to pain and allodynia, itch and alloknesis

Abstract

A model is proposed to explain the origins of two qualitatively different dysesthesias evoked by lightly stroking the skin surrounding a local cutaneous injury produced by different chemicals, one that evokes pain and another that elicits itch. Gently stroking the skin elicits pain (allodynia) after a pain-producing injection of capsaicin, but elicits itch (alloknesis) after an itch-producing injection of histamine. It is suggested that all primary sensory neurons that act to protect the body be called “nocifensor neurons” and that while some evoke sensations or reflexes that signal the occurrence of noxious events in peripheral tissue (“nociceptors”), others alter the properties of neuronal or non-neuronal tissue in the periphery or the central nervous system (“noceffectors”). The model proposes that pain and itch, produced, for example, by capsaicin and histamine, are evoked by activity in different populations of nociceptive primary afferent neurons that project onto two different types of spinothalamic tract cells in the dorsal horn. Allodynia and alloknesis are produced by other, different populations of noceffective primary afferents that act to produce a prolonged enhancement of activity in two different populations of interneurons in the dorsal horn. These interneurons receive a convergent input from low-threshold cutaneous mechanoreceptive afferents and project correspondingly onto the separate types of spinothalamic tract cells mediating pain or itch.