Voluntary alcohol consumption is controlled via the neuropeptide Y Y1 receptor.


Autoria(s): Thiele T.E.; Koh M.T.; Pedrazzini T.
Data(s)

2002

Resumo

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.

Identificador

https://serval.unil.ch/?id=serval:BIB_649506F5A988

isbn:1529-2401[electronic]

pmid:11826154

isiid:000173660800006

doi:

Idioma(s)

en

Fonte

Journal of Neuroscience, vol. 22, no. 3, pp. 208

Palavras-Chave #Alcohol Drinking; Alcoholic Intoxication; Animals; Behavior, Animal; Drug Resistance; Ethanol; Female; Male; Mice; Mice, Knockout; Motor Activity; Phenotype; Quinine; Receptors, Neuropeptide Y; Sex Factors; Sucrose
Tipo

info:eu-repo/semantics/article

article