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The Journal of Neuroscience, 0000, 20:RC75:1-6

RAPID COMMUNICATION
High Ethanol Consumption and Low Sensitivity to Ethanol-Induced Sedation in Protein Kinase A-Mutant Mice

Todd E. Thiele¹, Brandon Willis², Julia Stadler², James G. Reynolds¹, Ilene L. Bernstein¹, and G. Stanley McKnight²

¹ Department of Psychology and the Alcohol and Drug Abuse Institute and ² Department of Pharmacology, University of Washington, Seattle, Washington 98195

Both in vitro and in vivo evidence indicate that cAMP-dependent protein kinase (PKA) mediates some of the acute and chronic cellular responses to alcohol. However, it is unclear whether PKA regulates voluntary alcohol consumption. We therefore studied alcohol consumption by mice that completely lack the regulatory II (RII) subunit of PKA as a result of targeted gene disruption. Here we report that RII knockout mice (RII/) showed increased consumption of solutions containing 6, 10, and 20% (v/v) ethanol when compared with wild-type mice (RII+/+). On the other hand, RII/ mice showed normal consumption of solutions containing either sucrose or quinine. When compared with wild-type mice, the RII/ mice were found to be less sensitive to the sedative effects of ethanol as measured by more rapid recovery from ethanol-induced sleep, even though plasma ethanol concentrations did not differ significantly from those of controls. Finally, both RI- and catylatic subunit 1-deficient mice showed normal voluntary consumption of ethanol, indicating that increased ethanol consumption is not a general characteristic associated with deletion of PKA subunits. These data demonstrate a role for the RII subunit of PKA in regulating voluntary consumption of alcohol and sensitivity to the intoxication effects that are produced by this drug.

Key words: alcohol consumption; sedation; PKA; knock-out; regulatory subunit; intracellular signaling

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Copyright © 0000 Society for Neuroscience  0270-6474/00/$05.00/0

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