Molecular Mechanisms of Alcohol-Induced Analgesia -- Ethanol Directly Opens GIRK Channels --    Laboratory for Neurobiology of Emotion/ Laboratory for Cellular Information Processing  Researchers in one of the Cooperative Research Program of the RIKEN BSI, Laboratory for Neurobiology of Emotion (Lab. head, Dr. Hiroaki Niki), Laboratory for Cellular Information Processing (Lab. head, Dr. Ryoji Yano) and Brain Research Institute, Niigata University, and collaborated with Waseda University found that ethanol-induced analgesia is mediated by activations of G-protein-activated inwardly rectifying potassium channel (GIRK channel).   GIRK channels are highly expressed in the brain and heart and play an important role in regulation of neuronal activity and heart rate. In this study, they demonstrated that GIRK channels were activated by ethanol at pharmacologically relevant concentrations, by using Xenopus oocyte expression system and electrophysiological techniques. Furthermore, by using weaver mutant mice, having abnormal GIRK channel in the brain, they showed that the activation of GIRK channel by ethanol was involved in ethanol-induced analgesia. These findings provide not only important informations for understanding of ethanol effects on brain functions but also clues for development of novel medicine for ethanol addiction and analgesics targeting GIRK channels. Weaver mutant mice display similar jumping responses before and after ethanol administration, whereas normal mice show the responses with prolonged latencies after ethanol administration. Kobayashi, T., Ikeda, K., Kojima, H., Niki, H., Yano, R., Yoshioka, T., Kumanishi, T. Ethanol opens G-protein-activated inwardly rectifying K+ channels Nat. Neurosci. 2, 1091-1097, December (1999)