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

• Antragstellerin: Professorin Dr. Katharina Zimmermann
• Fachliche Zuordnung: Molekulare Biologie und Physiologie von Nerven- und Gliazellen
• Förderung: Förderung von 2007 bis 2008
• Projektkennung: Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 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-Verfahren: Forschungsstipendien
• Internationaler Bezug: USA
• Gastgeber: Professor David E. Clapham, Ph.D.