Capsaicin: actions on nociceptive C-fibres and therapeutic potential.
Recent work on the excitatory action of capsaicin on somatic and visceral afferent neurones shows that depolarization is selective for C-fibre polymodal nociceptor afferents and involves opening a non-selective cation channel. Exposure to significantly suprathreshold amounts of capsaicin causes permanent degeneration of C-fibre afferents in adult rats. Functional changes in rats (hypalgesia, diminished neurogenic inflammation) are likely to be a direct consequence of the loss of C-fibre nociceptors, and so are the reductions in neuropeptide levels that follow adult capsaicin treatment. Clinical trials of topical capsaicin treatment for post-herpetic neuralgia have yielded promising results. The selective nature of the action of capsaicin in reducing just C-nociceptor activity may make it particularly useful for treating pain states triggered by C-fibre input.
Lynn
Bruce
B
Department of Physiology, University College London,LondonU.K.
D000287:Administration, Topical; D000818:Animals; D002211:Capsaicin / Q000494:pharmacology* / Q000627:therapeutic use; D006566:Herpesviridae Infections / Q000503:physiopathology; D006801:Humans; D009407:Nerve Block; D009410:Nerve Degeneration; D009412:Nerve Fibers / Q000187:drug effects*; D009431:Neural Conduction / Q000187:drug effects; D009475:Neurons, Afferent / Q000187:drug effects; D009479:Neuropeptides / Q000378:metabolism; D009619:Nociceptors / Q000187:drug effects*; D010146:Pain / Q000188:drug therapy; D012867:Skin / Q000187:drug effects
D009479:Neuropeptides; D002211:Capsaicin