Sensitization of TRPV3 in keratinocytes versus sensory neurons as a mechanism of hyperalgesia

• Applicant: Professorin Dr. Katharina Zimmermann
• Subject Area: Molecular Biology and Physiology of Neurons and Glial Cells
• Term: from 2007 to 2008
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 36145580

The contribution of the heat-activated ion channels TRPV3 to the development ofinflammatory and neuropathic hyperalgesia will be investigated using tissue specificconditional knockout mice that lack TRPV3 in keratinocytes and/or DRGs. In vivobehavioural testing and pharmacology and in vitro electrophysiology on nativesensory neurons will be used to find out whether the lack of TRPV3 in eitherkeratinocytes and/or DRGs is responsible for the lack of inflammatory hyperalgesia,i.e. the published phenotype of general TRPV3 deficient mice. Techniques of cellularand molecular biology including also immunohistochemistry and laser TIRF will beused to investigate how sensitization of TRPV3 in either keratinocytes and /or DRGs.The expected findings will provide insight how noxious thermal stimuli are transducedin primary sensory neurons under basal, inflammatory and neuropathic conditions.

• DFG Programme: Research Fellowships
• International Connection: USA
• Host: Professor David E. Clapham, Ph.D.