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Research ArticleNEUROPHARMACOLOGY

Potassium Channels as Targets for Ethanol: Studies of G-Protein-Coupled Inwardly Rectifying Potassium Channel 2 (GIRK2) Null Mutant Mice

Yuri A. Blednov, M. Stoffel, S. R. Chang and R. Adron Harris
Journal of Pharmacology and Experimental Therapeutics August 2001, 298 (2) 521-530;
Yuri A. Blednov
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M. Stoffel
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S. R. Chang
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R. Adron Harris
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Abstract

G-Protein-coupled inwardly rectifying potassium channels (GIRKs) regulate synaptic transmission and neuronal firing rates. Selective enhancement of GIRK2 function by intoxicating concentrations of ethanol was recently shown for recombinant homomeric and heteromeric channels. We proposed that specific behavioral actions of ethanol are due to activation of GIRK channels and that these behaviors would be reduced or eliminated in GIRK2 null mutant (“knockout”) mice. Three behavioral effects of ethanol were absent in mutant mice as compared with wild-type littermates: stimulation of home cage (habituated) motor activity, anxiolytic action in elevated-plus maze test, and handling-induced convulsions (HIC) after an acute injection of ethanol. In contrast to these reductions of ethanol action, mutant mice displayed greater ethanol-stimulated activity in peripheral regions of an open field. There were no differences between mutant and wild-type mice for ethanol-induced sleep time, acute functional tolerance, or HIC following chronic matched consumption of a liquid diet. Ethanol preference and consumption were equal for wild-type and mutant mice using the standard two-bottle choice test with alternation of the bottles. However, this test was complicated by the strong side preference of the mice. When ethanol was presented constantly in their favored location, the consumption of ethanol was substantially higher for mutant than for wild-type mice. In the absence of ethanol, GIRK2 knockout mice showed more motor activity, less anxiety, and higher HIC. These results provide evidence that GIRK2 channels mediate specific behaviors, including anxiety and convulsions, and may influence effects of ethanol on these behaviors.

Footnotes

  • This work was supported by funds from the Texas Commission on Alcohol and Drug Abuse and National Institutes of Health/National Institute on Alcohol Abuse and Alcoholism Grants AA06399 and AA03527. A preliminary report of some of these results was presented at the 23rd Annual Scientific Meeting of Research Society on Alcoholism, Denver, CO, June 24–29, 2000.

  • Abbreviations:
    GIRK
    G-protein-coupled inwardly rectifying potassium channel
    HIC
    handling-induced convulsions
    ETOH
    ethanol
    BEC1 and BEC2
    initial and final blood ethanol concentrations, respectively
    ANOVA
    analysis of variance
    • Received April 30, 2001.
    • Accepted May 4, 2001.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 298 (2)
Journal of Pharmacology and Experimental Therapeutics
Vol. 298, Issue 2
1 Aug 2001
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Research ArticleNEUROPHARMACOLOGY

Potassium Channels as Targets for Ethanol: Studies of G-Protein-Coupled Inwardly Rectifying Potassium Channel 2 (GIRK2) Null Mutant Mice

Yuri A. Blednov, M. Stoffel, S. R. Chang and R. Adron Harris
Journal of Pharmacology and Experimental Therapeutics August 1, 2001, 298 (2) 521-530;

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Research ArticleNEUROPHARMACOLOGY

Potassium Channels as Targets for Ethanol: Studies of G-Protein-Coupled Inwardly Rectifying Potassium Channel 2 (GIRK2) Null Mutant Mice

Yuri A. Blednov, M. Stoffel, S. R. Chang and R. Adron Harris
Journal of Pharmacology and Experimental Therapeutics August 1, 2001, 298 (2) 521-530;
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