Capsazepine Inhibits Thermal Hyperalgesia but Not Nociception Triggered by Protease-Activated Receptor-2 in Rats

The Japanese Journal of Pharmacology

Chiho Shimada¹  Hideki Itoh¹  Atsufumi Kawabata¹  Ryotaro Kuroda¹  Naoyuki Kawao¹ 

[1] Department of Pathophysiology and Therapeutics, School of Pharmaceutical Sciences, Kinki University

关键词: Protease-activated receptor-2;    Capsazepine;    Pain;   

DOI  :  10.1254/jjp.89.184

学科分类：药理学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(15)Cited-By(20)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.

【 授权许可】

Unknown