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Publication : Neurobiological responses to ethanol in mutant mice lacking neuropeptide Y or the Y5 receptor.

First Author  Thiele TE Year  2000
Journal  Pharmacol Biochem Behav Volume  67
Issue  4 Pages  683-91
PubMed ID  11166058 Mgi Jnum  J:102529
Mgi Id  MGI:3607728 Doi  10.1016/s0091-3057(00)00413-5
Citation  Thiele TE, et al. (2000) Neurobiological responses to ethanol in mutant mice lacking neuropeptide Y or the Y5 receptor. Pharmacol Biochem Behav 67(4):683-91
abstractText  We have previously shown that voluntary ethanol consumption and resistance are inversely related to neuropeptide Y (NPY) levels in NPY-knockout (NPY -/-) and NPY-overexpressing mice. Here we report that NPY -/- mice on a mixed C57BL/6Jx129/SvEv background showed increased sensitivity to locomotor activation caused by intraperitoneal (ip) injection of 1.5 g/kg of ethanol, and were resistant to sedation caused by a 3.5-g/kg dose of ethanol. In contrast, NPY -/- mice on an inbred 129/SvEv background consumed the same amount of ethanol as wild-type (WT) controls at 3%, 6%, and 10% ethanol, but consumed significantly more of a 20% solution. They exhibited normal locomotor activation following a 1.5-g/kg injection of ethanol, and displayed normal sedation in response to 2.5 and 3.0 g/kg of ethanol, suggesting a genetic background effect. Y5 receptor knockout (Y5 -/-) mice on an inbred 129/SvEv background showed normal ethanol-induced locomotor activity and normal voluntary ethanol consumption, but displayed increased sleep time caused by 2.5 and 3.0 g/kg injection of ethanol. These data extend previous results by showing that NPY -/- mice of a mixed C57BL/6Jx129/SvEv background have increased sensitivity to the locomotor activation effect caused by a low dose of ethanol, and that expression of ethanol-related phenotypes are dependent on the genetic background of NPY -/- mice.
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