Vanilloid receptor-1 is essential for inflammatory thermal hyperalgesia

John B. Davis (), Julie Gray, Martin J. Gunthorpe, Jonathan P. Hatcher, Phil T. Davey, Philip Overend, Mark H. Harries, Judi Latcham, Colin Clapham, Kirsty Atkinson, Stephen A. Hughes, Kim Rance, Evelyn Grau, Alex J. Harper, Perdita L. Pugh, Derek C. Rogers, Sharon Bingham, Andrew Randall and Steven A. Sheardown
Additional contact information
Julie Gray: Departments of Neuroscience Research
Martin J. Gunthorpe: Departments of Neuroscience Research
Jonathan P. Hatcher: Departments of Neuroscience Research
Phil T. Davey: Departments of Neuroscience Research
Philip Overend: Statistical Sciences
Mark H. Harries: Departments of Neuroscience Research
Judi Latcham: Laboratory Animal Sciences
Colin Clapham: Biotechnology & Genetics, SmithKline Beecham Pharmaceuticals
Kirsty Atkinson: Biotechnology & Genetics, SmithKline Beecham Pharmaceuticals
Stephen A. Hughes: Biotechnology & Genetics, SmithKline Beecham Pharmaceuticals
Kim Rance: Biotechnology & Genetics, SmithKline Beecham Pharmaceuticals
Evelyn Grau: Biotechnology & Genetics, SmithKline Beecham Pharmaceuticals
Alex J. Harper: Departments of Neuroscience Research
Perdita L. Pugh: Departments of Neuroscience Research
Derek C. Rogers: Departments of Neuroscience Research
Sharon Bingham: Departments of Neuroscience Research
Andrew Randall: Departments of Neuroscience Research
Steven A. Sheardown: Biotechnology & Genetics, SmithKline Beecham Pharmaceuticals

Nature, 2000, vol. 405, issue 6783, 183-187

Abstract: Abstract The vanilloid receptor-1 (VR1) is a ligand-gated, non-selective cation channel expressed predominantly by sensory neurons. VR1 responds to noxious stimuli including capsaicin, the pungent component of chilli peppers, heat and extracellular acidification, and it is able to integrate simultaneous exposure to these stimuli1,2. These findings and research linking capsaicin with nociceptive behaviours (that is, responses to painful stimuli in animals3 have led to VR1 being considered as important for pain sensation. Here we have disrupted the mouse VR1 gene using standard gene targeting techniques. Small diameter dorsal root ganglion neurons isolated from VR1-null mice lacked many of the capsaicin-, acid- and heat-gated responses that have been previously well characterized in small diameter dorsal root ganglion neurons from various species. Furthermore, although the VR1-null mice appeared normal in a wide range of behavioural tests, including responses to acute noxious thermal stimuli, their ability to develop carrageenan-induced thermal hyperalgesia was completely absent. We conclude that VR1 is required for inflammatory sensitization to noxious thermal stimuli but also that alternative mechanisms are sufficient for normal sensation of noxious heat.

Date: 2000
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DOI: 10.1038/35012076

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