That the receptor for capsaicin is involved in pain is intuitively attractive to even the lay person. After all, who among us has not had the misfortune of inadvertently ingesting an excess dose of chili pepper, and suddenly had the pleasure of a restaurant meal transformed into flushing, diaphoresis and instant agony. Since the identification of the receptor for capsaicin, TRPV1 (Tominaga et al. 1998), and its localization to sensory neurons, there has been a virtual explosion of research into its roles in the production of pain. It has recently become recognized that induction of pain by nerve damage or inflammation involves changes in the function of primary sensory neurons (plasticity), and that these changes often involve alteration in the expression or function of a variety of types of ion channels (Beyak & Vanner, 2005). Therefore an ion channel that normally is responsible for the detection of noxious thermal stimuli is a prime target as the culprit in the development of pathological pain.
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