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Article
Nature 389, 816-824 (23 October 1997) | doi:10.1038/39807; Received 20 August 1997; Accepted 24 September 1997
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The capsaicin receptor: a heat-activated ion channel in the pain pathway
Michael J. Caterina1, Mark A. Schumacher2,3, Makoto Tominaga1,3, Tobias A. Rosen1, Jon D. Levine4 & David Julius1
- Departments of Cellular and Molecular Pharmacology, San Francisco, California 94143-0450, USA
- Departments of Anesthesia, San Francisco, California 94143-0450, USA
- Departments of Medicine, University of California, San Francisco, California 94143-0450, USA
- These authors contributed equally to this study.
Correspondence to: David Julius1 Correspondence and requests for materials should be made to D.J. (e-mail: Email: julius@socrates.ucsf.edu). The Genbank accession number for VR1 is AF029310.
Abstract
Capsaicin, the main pungent ingredient in 'hot' chilli peppers, elicits a sensation of burning pain by selectively activating sensory neurons that convey information about noxious stimuli to the central nervous system. We have used an expression cloning strategy based on calcium influx to isolate a functional cDNA encoding a capsaicin receptor from sensory neurons. This receptor is a non-selective cation channel that is structurally related to members of the TRP family of ion channels. The cloned capsaicin receptor is also activated by increases in temperature in the noxious range, suggesting that it functions as a transducer of painful thermal stimuli in vivo.
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