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Abstract
The capsaicin (vanilloid) receptor VR1 is a cation channel expressed by primary sensory neurons of the “pain” pathway. Heterologously expressed VR1 can be activated by vanilloid compounds, protons, or heat (>43°C), but whether this channel contributes to chemical or thermal sensitivity in vivo is not known. Here, we demonstrate that sensory neurons from mice lacking VR1 are severely deficient in their responses to each of these noxious stimuli. VR1−/− mice showed normal responses to noxious mechanical stimuli but exhibited no vanilloid-evoked pain behavior, were impaired in the detection of painful heat, and showed little thermal hypersensitivity in the setting of inflammation. Thus, VR1 is essential for selective modalities of pain sensation and for tissue injury–induced thermal hyperalgesia.
↵* Present address: Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
↵† Present address: Neurobiology Unit, Roche Bioscience, Palo Alto, CA 94304–1397, USA.
↵‡ Present address: Merck Research Laboratories, Rahway, NJ 07065, USA.
↵§ To whom correspondence should be addressed. E-mail: julius{at}socrates.ucsf.edu
