Inflammatory pain: The cellular basis of heat hyperalgesia

被引:146
作者
Huang, Jiehong [1 ]
Zhang, Xuming [1 ]
McNaughton, Peter A. [1 ]
机构
[1] Univ Cambridge, Dept Pharmacol, Cambridge CB2 1PD, England
基金
英国生物技术与生命科学研究理事会;
关键词
pain; sensory transduction; inflammation; protein kinase; intracellular signalling; capsaicin; heat; TRPV1;
D O I
10.2174/157015906778019554
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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.
引用
收藏
页码:197 / 206
页数:10
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