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The Journal of Neuroscience, 2002, 22:RC208:1-6

RAPID COMMUNICATION
Voluntary Alcohol Consumption Is Controlled via the Neuropeptide Y Y1 Receptor

Todd E. Thiele¹, Ming Teng Koh², and Thierry Pedrazzini³

¹ Department of Psychology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-3270, ² Department of Psychology and the Alcohol and Drug Abuse Institute, University of Washington, Seattle, Washington 98195, and ³ Division of Hypertension, University of Lausanne Medical School, CH-1011 Lausanne, Switzerland

We have shown previously that voluntary ethanol consumption and resistance to ethanol-induced sedation are inversely related to neuropeptide Y (NPY) levels in NPY-knock-out (NPY^/) and NPY-overexpressing mice. In the present report, we studied knock-out mice completely lacking the NPY Y1 receptor (Y1^/) to further characterize the role of the NPY system in ethanol consumption and neurobiological responses to this drug. Here we report that male Y1^/ mice showed increased consumption of solutions containing 3, 6, and 10% (v/v) ethanol when compared with wild-type (Y1^+/+) control mice. Female Y1^/ mice showed increased consumption of a 10% ethanol solution. In contrast, Y1^/ mice showed normal consumption of solutions containing either sucrose or quinine. Relative to Y1^+/+ mice, male Y1^/ mice were found to be less sensitive to the sedative effects of 3.5 and 4.0 gm/kg ethanol as measured by more rapid recovery from ethanol-induced sleep, although plasma ethanol levels did not differ significantly between the genotypes. Finally, male Y1^/ mice showed normal ethanol-induced ataxia on the rotarod test after administration of a 2.5 gm/kg dose. These data suggest that the NPY Y1 receptor regulates voluntary ethanol consumption and some of the intoxicating effects caused by administration of ethanol.

Key words: alcohol consumption; sedation; NPY; receptor; knock-out; ataxia

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

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