GABA puts the brakes on TRPV1

At the Institute of Pharmacology, CellNetworks member and SFB1158 PI 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.

Find out more about the research on their lab website.

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