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Inflammatory pain: the cellular basis of heat hyperalgesia.

Authors
  • Huang, Jiehong1
  • Zhang, Xuming
  • McNaughton, Peter A
  • 1 Department of Pharmacology, University of Cambridge, Cambridge, CB2 1PD, United Kingdom. , (United Kingdom)
Type
Published Article
Journal
Current Neuropharmacology
Publisher
Bentham Science
Publication Date
Jul 01, 2006
Volume
4
Issue
3
Pages
197–206
Identifiers
PMID: 18615146
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Injury or inflammation release a range of inflammatory mediators that increase the sensitivity of sensory neurons to noxious thermal or mechanical stimuli. The heat- and capsaicin-gated channel TRPV1, which is an important detector of multiple noxious stimuli, plays a critical role in the development of thermal hyperalgesia induced by a wide range of inflammatory mediators. We review here recent findings on the molecular mechanisms of sensitisation of TRPV1 by inflammatory mediators, including bradykinin, ATP, NGF and prostaglandins. We describe the signalling pathways believed to be involved in the potentiation of TRPV1, and our current understanding of how inflammatory mediators couple to these pathways.

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