Capsazepine inhibits thermal hyperalgesia but not nociception triggered by protease-activated receptor-2 in rats.
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.
Department of Pathophysiology and Therapeutics, School of Pharmaceutical Sciences, Kinki University, Higashi-Osaka, Japan.
Naoyuki
N
Kawao
Chiho
C
Shimada
Hideki
H
Itoh
Ryotaro
R
Kuroda
Atsufumi
A
Kawabata
D000595:Amino Acid Sequence; D000818:Animals; D002211:Capsaicin / Q000031:analogs & derivatives* / Q000494:pharmacology* / Q000627:therapeutic use; D006358:Hot Temperature; D006930:Hyperalgesia / Q000139:chemically induced*; D008297:Male; D010146:Pain / Q000139:chemically induced / Q000188:drug therapy*; D010446:Peptide Fragments / Q000737:chemistry / Q000633:toxicity*; D051381:Rats; D017208:Rats, Wistar; D044464:Receptor, PAR-2; D018179:Receptors, Thrombin / Q000737:chemistry*
D010446:Peptide Fragments; D044464:Receptor, PAR-2; D018179:Receptors, Thrombin; C071423:capsazepine; D002211:Capsaicin