Capsaicin-containing topical analgesics appear to achieve their action through their agonist activity at the transient receptor potential of vanilloid receptor 1 (TRPV1) on Adelta and C-fibers.12[V], 13[V] This results in the release of substance P, as well as calcitonin gene-related peptide (CGRP). Therapeutic responses to capsaicin are generally achieved only with repeated topical application. It has been suggested that reduced peripheral, as well as central excitability with resulting less pain through reduced afferent input, is the outcome of the depletion of substance P in C fibers.7[III], 12[V], 13[V] Histopathological examination results of human nerve biopsies, as well as of animal experiments, have suggested that application of capsaicin may lead to nerve fiber degeneration in the skin underneath the site of application. This neurodegenera-tive effect of capsaicin has been hypothesized to be one of its mechanisms of pain relief.14[III]

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