Abstract
Discovery of heat-activated ion channels and of the vanilloid receptors VR1 and VRL 1 in sensory neurons of the spinal ganglion has shed new light on the transduction mechanisms by which inflammatory mediators and chemical irritants excite nociceptors and contribute to pain. Prostaglandin E2, histamine and, most potently, bradykinin and low pH as well as capsaicin and phorbol esters induce a prominent sensitization to heat of nociceptors including recruitment of previously unresponsive receptor terminals. Various membrane bound receptors and alternative second-messenger pathways, including PKC, cAMP and calcium influx, are involved in the transduction of the sensitizing effect. Putative heat-sensitive ion channels, including the vanilloid receptors, are the targets of the sensitizing action which is probably mediated by protein phosphorylation.
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