| First Author | Thiele TE | Year | 2002 |
| Journal | J Neurosci | Volume | 22 |
| Issue | 3 | Pages | RC208 |
| PubMed ID | 11826154 | Mgi Jnum | J:109207 |
| Mgi Id | MGI:3626119 | Doi | 10.1523/JNEUROSCI.22-03-j0006.2002 |
| Citation | Thiele TE, et al. (2002) Voluntary alcohol consumption is controlled via the neuropeptide Y Y1 receptor. J Neurosci 22(3):RC208 |
| abstractText | 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. |
