Author: ["N. Vergnolle","N.W. Bunnett","K.A. Sharkey","V. Brussee","S.J. Compton","E.F. Grady","G. Cirino","N. Gerard","A.I. Basbaum","P. Andrade-Gordon","M.D. Hollenberg","J.L. Wallace"]
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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.Cite this article
Vergnolle, N., Bunnett, N., Sharkey, K. et al. Proteinase-activated receptor-2 and hyperalgesia: A novel pain pathway. Nat Med 7, 821–826 (2001). https://doi.org/10.1038/89945 