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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

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.[1]

References

  1. Capsazepine inhibits thermal hyperalgesia but not nociception triggered by protease-activated receptor-2 in rats. Kawao, N., Shimada, C., Itoh, H., Kuroda, R., Kawabata, A. Jpn. J. Pharmacol. (2002) [Pubmed]
 
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