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, sensory transduction, inflammation, protein kinase, intracellular signalling, capsaicin, heat, TRPV1
Current Neuropharmacology
Title: Inflammatory Pain: The Cellular Basis of Heat Hyperalgesia
Volume: 4 Issue: 3
Author(s): Jiehong Huang, Xuming Zhang and Peter A. McNaughton
Affiliation:
Keywords: Pain, sensory transduction, inflammation, protein kinase, intracellular signalling, capsaicin, heat, TRPV1
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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Cite this article as:
Huang Jiehong, Zhang Xuming and McNaughton A. Peter, Inflammatory Pain: The Cellular Basis of Heat Hyperalgesia, Current Neuropharmacology 2006; 4 (3) . https://dx.doi.org/10.2174/157015906778019554
DOI https://dx.doi.org/10.2174/157015906778019554 |
Print ISSN 1570-159X |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6190 |
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