Impaired Nociception and Pain Sensation in Mice Lacking the Capsaicin Receptor

DOI Web Site 被引用文献151件
  • M. J. Caterina
    Department of Cellular and Molecular Pharmacology,
  • A. Leffler
    Department of Neurology, University of Würzburg, D-97080 Würzburg, Germany.
  • A. B. Malmberg
    Departments of Anatomy and Physiology and the W. M. Keck Center for Neuroscience, University of California, San Francisco, San Francisco, CA 94143–0450, USA.
  • W. J. Martin
    Departments of Anatomy and Physiology and the W. M. Keck Center for Neuroscience, University of California, San Francisco, San Francisco, CA 94143–0450, USA.
  • J. Trafton
    Departments of Anatomy and Physiology and the W. M. Keck Center for Neuroscience, University of California, San Francisco, San Francisco, CA 94143–0450, USA.
  • K. R. Petersen-Zeitz
    Departments of Anatomy and Physiology and the W. M. Keck Center for Neuroscience, University of California, San Francisco, San Francisco, CA 94143–0450, USA.
  • M. Koltzenburg
    Department of Neurology, University of Würzburg, D-97080 Würzburg, Germany.
  • A. I. Basbaum
    Departments of Anatomy and Physiology and the W. M. Keck Center for Neuroscience, University of California, San Francisco, San Francisco, CA 94143–0450, USA.
  • D. Julius
    Department of Cellular and Molecular Pharmacology,

書誌事項

公開日
2000-04-14
DOI
  • 10.1126/science.288.5464.306
公開者
American Association for the Advancement of Science (AAAS)

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説明

<jats:p> 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 <jats:sup>−/−</jats:sup> 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. </jats:p>

収録刊行物

  • Science

    Science 288 (5464), 306-313, 2000-04-14

    American Association for the Advancement of Science (AAAS)

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