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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