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Ethanol opens G-protein-activated inwardly rectifying K+ channels
doi: 10.1038/16019
pmid: 10570486
Ethanol affects many functions of the brain and peripheral organs. Here we show that ethanol opens G-protein-activated, inwardly rectifying K + (GIRK) channels, which has important implications for inhibitory regulation of neuronal excitability and heart rate. At pharmacologically relevant concentrations, ethanol activated both brain-type GIRK1/2 and cardiac-type GIRK1/4 channels without interaction with G proteins or second messengers. Moreover, weaver mutant mice, which have a missense mutation in the GIRK2 channel, showed a loss of ethanol-induced analgesia. These results suggest that the GIRK channels in the brain and heart are important target sites for ethanol.
- Waseda University Japan
- RIKEN Japan
- Niigata University Japan
- Niigata University Japan
Patch-Clamp Techniques, Potassium Channels, Mutation, Missense, Receptors, Opioid, mu, Motor Activity, Mice, Animals, Potassium Channels, Inwardly Rectifying, Pain Measurement, Mice, Inbred C3H, Ethanol, Myocardium, Brain, Heterotrimeric GTP-Binding Proteins, Mice, Mutant Strains, G Protein-Coupled Inwardly-Rectifying Potassium Channels, Alcohols, Oocytes, Potassium, Ion Channel Gating
Patch-Clamp Techniques, Potassium Channels, Mutation, Missense, Receptors, Opioid, mu, Motor Activity, Mice, Animals, Potassium Channels, Inwardly Rectifying, Pain Measurement, Mice, Inbred C3H, Ethanol, Myocardium, Brain, Heterotrimeric GTP-Binding Proteins, Mice, Mutant Strains, G Protein-Coupled Inwardly-Rectifying Potassium Channels, Alcohols, Oocytes, Potassium, Ion Channel Gating
