Proteinase-activated receptor-2 and hyperalgesia: A novel pain pathway.
Nat Med
; 7(7): 821-6, 2001 Jul.
Article
em En
| MEDLINE
| ID: mdl-11433347
ABSTRACT
Using a combined pharmacological and gene-deletion approach, we have delineated a novel mechanism of neurokinin-1 (NK-1) receptor-dependent hyperalgesia induced by proteinase-activated receptor-2 (PAR2), a G-protein-coupled receptor expressed on nociceptive primary afferent neurons. Injections into the paw of sub-inflammatory doses of PAR2 agonists in rats and mice induced a prolonged thermal and mechanical hyperalgesia and elevated spinal Fos protein expression. This hyperalgesia was markedly diminished or absent in mice lacking the NK-1 receptor, preprotachykinin-A or PAR2 genes, or in rats treated with a centrally acting cyclooxygenase inhibitor or treated by spinal cord injection of NK-1 antagonists. Here we identify a previously unrecognized nociceptive pathway with important therapeutic implications, and our results point to a direct role for proteinases and their receptors in pain transmission.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Dor
/
Receptores de Trombina
/
Hiperalgesia
Limite:
Animals
Idioma:
En
Ano de publicação:
2001
Tipo de documento:
Article