Proton block of proton-activated TRPV1 current.

ABSTRACT: The TRPV1 cation channel is a polymodal nociceptor that is activated by heat and ligands such as capsaicin and is highly sensitive to changes in extracellular pH. In the body core, where temperature is usually stable and capsaicin is normally absent, H(+) released in response to ischemia, tissue injury, or inflammation is the best-known endogenous TRPV1 agonist, activating the channel to mediate pain and vasodilation. Paradoxically, removal of H(+) elicits a transient increase in TRPV1 current that is much larger than the initial H(+)-activated current. We found that this prominent OFF response is caused by rapid recovery from H(+) inhibition of the excitatory current carried by H(+)-activated TRPV1 channels. H(+) inhibited current by interfering with ion permeation. The degree of inhibiti

SUBMITTER: Lee BH 

PROVIDER: S-EPMC4516785 | biostudies-literature | 2015 Aug

REPOSITORIES: biostudies-literature