{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1362825894737412352.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1126/science.288.5464.306"}},{"identifier":{"@type":"URI","@value":"https://www.science.org/doi/pdf/10.1126/science.288.5464.306"}},{"identifier":{"@type":"NAID","@value":"80011834683"}}],"dc:title":[{"@value":"Impaired Nociception and Pain Sensation in Mice Lacking the Capsaicin Receptor"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p>\n            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\n            <jats:sup>−/−</jats:sup>\n            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.\n          </jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1581417126697265664","@type":"Researcher","foaf:name":[{"@value":"M. J. Caterina"}],"jpcoar:affiliationName":[{"@value":"Department of Cellular and Molecular Pharmacology,"}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894737412357","@type":"Researcher","foaf:name":[{"@value":"A. Leffler"}],"jpcoar:affiliationName":[{"@value":"Department of Neurology, University of Würzburg, D-97080 Würzburg, Germany."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894737412358","@type":"Researcher","foaf:name":[{"@value":"A. B. Malmberg"}],"jpcoar:affiliationName":[{"@value":"Departments of Anatomy and Physiology and the W. M. Keck Center for Neuroscience, University of California, San Francisco, San Francisco, CA 94143–0450, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894737412354","@type":"Researcher","foaf:name":[{"@value":"W. J. Martin"}],"jpcoar:affiliationName":[{"@value":"Departments of Anatomy and Physiology and the W. M. Keck Center for Neuroscience, University of California, San Francisco, San Francisco, CA 94143–0450, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894737412356","@type":"Researcher","foaf:name":[{"@value":"J. Trafton"}],"jpcoar:affiliationName":[{"@value":"Departments of Anatomy and Physiology and the W. M. Keck Center for Neuroscience, University of California, San Francisco, San Francisco, CA 94143–0450, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894737412360","@type":"Researcher","foaf:name":[{"@value":"K. R. Petersen-Zeitz"}],"jpcoar:affiliationName":[{"@value":"Departments of Anatomy and Physiology and the W. M. Keck Center for Neuroscience, University of California, San Francisco, San Francisco, CA 94143–0450, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894737412352","@type":"Researcher","foaf:name":[{"@value":"M. Koltzenburg"}],"jpcoar:affiliationName":[{"@value":"Department of Neurology, University of Würzburg, D-97080 Würzburg, Germany."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894737412353","@type":"Researcher","foaf:name":[{"@value":"A. I. Basbaum"}],"jpcoar:affiliationName":[{"@value":"Departments of Anatomy and Physiology and the W. M. Keck Center for Neuroscience, University of California, San Francisco, San Francisco, CA 94143–0450, USA."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894737412359","@type":"Researcher","foaf:name":[{"@value":"D. Julius"}],"jpcoar:affiliationName":[{"@value":"Department of Cellular and Molecular Pharmacology,"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"00368075"},{"@type":"EISSN","@value":"10959203"}],"prism:publicationName":[{"@value":"Science"}],"dc:publisher":[{"@value":"American Association for the Advancement of Science (AAAS)"}],"prism:publicationDate":"2000-04-14","prism:volume":"288","prism:number":"5464","prism:startingPage":"306","prism:endingPage":"313"},"reviewed":"false","url":[{"@id":"https://www.science.org/doi/pdf/10.1126/science.288.5464.306"}],"createdAt":"2002-07-27","modifiedAt":"2024-01-13","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1050009640108985472","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Implications of Transient Receptor Potential Cation Channels in Migraine 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behavior"}]},{"@id":"https://cir.nii.ac.jp/crid/1050851165478874880","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Striatal TRPV1 activation by acetaminophen ameliorates dopamine D2 receptor antagonists-induced orofacial dyskinesia"},{"@value":"Striatal TRPV1 activation by acetaminophen ameliorates dopamine D2 receptor antagonist–induced orofacial dyskinesia"}]},{"@id":"https://cir.nii.ac.jp/crid/1360002216797292544","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Intrathecal AAV Serotype 9-mediated Delivery of shRNA Against TRPV1 Attenuates Thermal Hyperalgesia in a Mouse Model of Peripheral Nerve Injury"}]},{"@id":"https://cir.nii.ac.jp/crid/1360004230167613952","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Involvement of 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