Capsazepine inhibits thermal hyperalgesia but not nociception triggered by protease-activated receptor-2 in rats.

Abstract

Protease-activated receptor-2 (PAR-2), expressed in sensory neurons, triggers thermal hyperalgesia, nociceptive behavior and spinal Fos expression in rats. In the present study, we examined if the nociceptive processing by PAR-2 is mediated by trans-activation of capsaicin receptors. The thermal hyperalgesia following an intraplantar (i.pl.) administration of the PAR-2-activating peptide SLIGRL-NH2 was completely abolished by the capsaicin receptor antagonist capsazepine. In contrast, neither the nociceptive behavior nor spinal Fos expression in response to i.pl. SLIGRL-NH2 were attenuated by capsazepine. Our data imply that trans-activation of capsaicin receptors by PAR-2 might be involved in the PAR-2-triggered thermal hyperalgesia, but not nociception.