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Published on Sep 6, 2016
Heidelberg University: At the Institute of Pharmacology, CellNetworks member Prof. Jan Siemens and his research group explore sensory mechanisms at the molecular level. In their paper, published in Cell in 2015, they discovered a molecular mechanism in nerve cells which reverts the sensitized state of the capsaicin receptor TRPV1. With the activiation of GABAB1, the receptor forms a complex with TRPV1 to counteract inflammatory pain. Harnessing this mechanism for anti-pain therapy may prevent adverse effects associated with currently availabe TRPV1 blockers.