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Publication : Impaired nociception and pain sensation in mice lacking the capsaicin receptor.

First Author  Caterina MJ Year  2000
Journal  Science Volume  288
Issue  5464 Pages  306-13
PubMed ID  10764638 Mgi Jnum  J:61534
Mgi Id  MGI:1355140 Doi  10.1126/science.288.5464.306
Citation  Caterina MJ, et al. (2000) Impaired nociception and pain sensation in mice lacking the capsaicin receptor [see comments]. Science 288(5464):306-13
abstractText  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 degrees 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.
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