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

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Author(s)

    • KURODA Ryotaro
    • Department of Pathophysiology and Therapeutics, School of Pharmaceutical Sciences, Kinki University
    • KAWABATA Atsufumi
    • Department of Pathophysiology and Therapeutics, School of Pharmaceutical Sciences, Kinki University

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-NH<sub>2</sub> 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-NH<sub>2</sub> 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.

Journal

  • The Japanese Journal of Pharmacology

    The Japanese Journal of Pharmacology 89(2), 184-187, 2002-06-01

    The Japanese Pharmacological Society

References:  15

Cited by:  3

Codes

  • NII Article ID (NAID)
    10008684221
  • NII NACSIS-CAT ID (NCID)
    AA00691188
  • Text Lang
    ENG
  • Article Type
    Journal Article
  • ISSN
    00215198
  • NDL Article ID
    6262108
  • NDL Source Classification
    ZS51(科学技術--薬学)
  • NDL Call No.
    Z53-D199
  • Data Source
    CJP  CJPref  NDL  J-STAGE 
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