Abstract

This article gives a brief account of the neuropharmacological properties and pathophysiological implications of sensory neurons that are sensitive to the neurotoxin capsaicin. The exceptional selectivity with which this drug acts on a population of fine primary afferent neurons has made capsaicin an important research tool in sensory neuroscience. Capsaicinsensitive afferent neurons are sensory neurons with small-diameter somata and unmyelinated or thinly myelinated axons. They contain a number of neuropeptide transmitters including substance P and calcitonin gene-related peptide. According to the sensory modalities they perceive, capsaicinsensitive afferent neurons are mostly polymodal nociceptors and warm receptors. Characteristically these neurons subserve a dual afferent and local effector role. The afferent function enables information to be conveyed to the central nervous system. The local effector function arises from the release of neuropeptide transmitters from the peripheral nerve terminals of sensory neurons, these peptides governing many local tissue processes, notably vasodilatation. Both the afferent and local effector functions of sensory neurons enable the organism to react adequately to changes in its internal and external environment and to maintain homeostasis. Capsaicin treatment thus provides an experimental model of a sensory neuropathy with which to study the morphological, neurochemical and functional consequences of ablation of a defined group of afferent neurons. This model has considerable potential for the diagnosis, pathophysiology and treatment of disorders of the sensory nervous system in man.

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