Inflammatory Pain: The Cellular Basis of Heat Hyperalgesia

Author(s): Jiehong Huang, Xuming Zhang, Peter A. McNaughton

Journal Name: Current Neuropharmacology

Volume 4 , Issue 3 , 2006

Become EABM
Become Reviewer
Call for Editor


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, sensory transduction, inflammation, protein kinase, intracellular signalling, capsaicin, heat, TRPV1

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2006
Page: [197 - 206]
Pages: 10
DOI: 10.2174/157015906778019554
Price: $65

Article Metrics

PDF: 1