Inflammatory pain: the cellular basis of heat hyperalgesia

Jiehong Huang, Xuming Zhang, Peter A McNaughton

Research output: Contribution to journalArticle

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.

Original languageEnglish
Pages (from-to)197-206
Number of pages10
JournalCurrent Neuropharmacology
Volume4
Issue number3
Publication statusPublished - Jul 2006

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Hyperalgesia
Hot Temperature
Pain
Capsaicin
Bradykinin
Nerve Growth Factor
Sensory Receptor Cells
Prostaglandins
Adenosine Triphosphate
Inflammation
Wounds and Injuries

Keywords

  • Journal Article

Cite this

Huang, Jiehong ; Zhang, Xuming ; McNaughton, Peter A. / Inflammatory pain : the cellular basis of heat hyperalgesia. In: Current Neuropharmacology. 2006 ; Vol. 4, No. 3. pp. 197-206.
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Huang, J, Zhang, X & McNaughton, PA 2006, 'Inflammatory pain: the cellular basis of heat hyperalgesia', Current Neuropharmacology, vol. 4, no. 3, pp. 197-206.

Inflammatory pain : the cellular basis of heat hyperalgesia. / Huang, Jiehong; Zhang, Xuming; McNaughton, Peter A.

In: Current Neuropharmacology, Vol. 4, No. 3, 07.2006, p. 197-206.

Research output: Contribution to journalArticle

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T2 - the cellular basis of heat hyperalgesia

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AU - Zhang, Xuming

AU - McNaughton, Peter A

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M3 - Article

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EP - 206

JO - Current Neuropharmacology

JF - Current Neuropharmacology

SN - 1570-159X

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