Abstract
TRPV1 is a nonselective calcium permeable cation channel present in polymodal nociceptors that plays a crucial role in the development of inflammatory pain and thermal hypersensitivity. Plasmamembrane phosphoinositides are recognized as important regulators of TRPV1; the precise nature of their effect is, however, controversial. Recent studies indicate that phosphatidyl inositol (4,5) bisphosphate [PI(4,5)P2] and other phosphoinositides activate TRPV1 in excised patches. In concert with previous studies, we have shown that calcium influx-mediated activation of PLC results in a robust depletion of both phosphatidyl inositol (4) phosphate [PI(4)P] and PI(4,5)P2 and is one of the mechanisms of TRPV1 desensitization.
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