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PMID: 18615146 Published · ppublish English Journal Article

Inflammatory pain: the cellular basis of heat hyperalgesia.

Current neuropharmacology ·Vol. 4 ·No. 3 ·2006-07-00 ·Pages 197-206

Huang J, Zhang X, McNaughton PA

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.

Keywords
Pain TRPV1 capsaicin heat inflammation intracellular signalling protein kinase sensory transduction
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Huang Jiehong
Department of Pharmacology, University of Cambridge, Cambridge, CB2 1PD, United Kingdom.
Zhang Xuming
McNaughton Peter A
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Article Info
Journal
Current neuropharmacology
Abbr.
Curr Neuropharmacol
ISSN
1570-159X
Published
2006-07-00
Pages
197-206
Language
English
Region
United Arab Emirates
NLM ID
101157239
PMCID
PMC2430694
Grants
Biotechnology and Biological Sciences Research Council · BB/C003217/1 · United Kingdom
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