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Capsaicin (CAP)-activated ion channel plays a key role in generating nociceptive neural signals in sensory neurons. Here we present evidence that intracellular ATP upregulates the activity of capsaicin receptor channel. In inside-out membrane patches isolated from sensory neurons, application of CAP activated a nonselective cation channel (icap). Further addition of ATP to the bath caused a significant increase inicap , with aK1/2 of 3.3 mm. Nonhydrolyzable analogs of ATP, adenylimidodiphosphate and adenosine 5′-O-(3-thio)-triphosphate, also increasedicap . Neither Mg2+-free medium nor inhibitors of various kinases blocked the increase in icap induced by ATP. The enhancing effect of ATP was also observed in inside-out patches of oocytes expressing vanilloid receptor 1, a cloned capsaicin receptor. Single point mutations (D178N, K735R) within the putative Walker type nucleotide-binding domains abolished the effect of ATP. These results show that ATP increasesicap in sensory neurons by direct interaction with the CAP channel without involvement of phosphorylation.

Intracellular ATP Increases Capsaicin-Activated Channel Activity by Interacting with Nucleotide-Binding Domains