Peripheral PAR-2 triggers thermal hyperalgesia and nociceptive responses in rats.

Abstract:

:Protease-activated receptor-2 (PAR-2), a member of the G protein-coupled, seven trans-membrane domain receptor family, is activated by trypsin/tryptase and present in various tissues including the primary sensory neurons, playing a role in development of neurogenic inflammation. The present study examined if activation of peripheral PAR-2 could modulate nociception in the rat. Expression of mRNA for PAR-2 was confirmed in the L4-6 dorsal root ganglia, but not spinal cord. The PAR-2-activating peptide SLIGRL-NH2 administered by the intraplantar (i.pl.) route, produced thermal, but not mechanical, hyperalgesia in the rat, although the PAR-2-inactive control peptide LSIGRL-NH2 had no effect. Not only the PAR-2-activating but also inactive peptides elicited nociceptive behavior (licking/biting) in the intact rats, whereas only the former peptide produced such behavior in the rats that had received repeated administration of compound 48/80 for mast cell depletion. These data provide novel evidence that activation of peripheral PAR-2 is pro-nociceptive, producing thermal hyperalgesia and also triggering pain sensation, by itself, independently of mast cell degranulation.

journal_name

Neuroreport

journal_title

Neuroreport

authors

Kawabata A,Kawao N,Kuroda R,Tanaka A,Itoh H,Nishikawa H

doi

10.1097/00001756-200103260-00020

subject

Has Abstract

pub_date

2001-03-26 00:00:00

pages

715-9

issue

4

eissn

0959-4965

issn

1473-558X

journal_volume

12

pub_type

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