Assessment of ethanol consumption and water drinking by NPYY2 receptor knockout mice

作者：Thiele TE^*; Naveilhan P; Ernfors P

来源：Peptides, 2004, 25(6): 975-983.

DOI：10.1016/j.peptide.2004.03.009

• neuropeptide Y
• Y-2
• receptor
• alcohol consumption
• water consumption
• knockout
• mice

In recent years, pharmacological and genetic evidence have emerged suggesting that neuropeptide Y (NPY) and the NPY Y-1 receptor are involved with neurobiological responses to ethanol. Pharmacological data implicate a role for the NPY Y-2 receptor in ethanol self-administration. The purpose of the present study was to determine if genetic mutation of the Y-2 receptor would modulate ethanol consumption and/or ethanol-induced sedation. Here, we report that mutant mice lacking the NPY Y-2 receptor (Y-2(-/-)), when maintained on a mixed 50% 129/SvJ x 50% Balb/cJ background, drink significantly less of solutions containing 3 or 6% (v/v) ethanol relative to wild-type (Y-2(+/+)) mice. These mice drink normal amounts of solutions containing sucrose or quinine, have normal blood ethanol clearance, and show normal sensitivity to ethanol-induced sedation. However, Y-2(-/-) mice that are backcrossed to a Balb/cJ background show normal consumption of ethanol, indicating that the contributions of the NPY Y-2 receptor to ethanol consumption are genetic background dependent. Consistent with previous data Suggesting that NPY modulates water drinking, Y-2(-/-) mice of both genetic backgrounds consume significantly more water than Y-2(+/+) mice. The present results suggest roles for the NPY Y-2 receptor in the modulation of ethanol and water consumption.

• 出版日期2004-6