The alcohol-induced locomotor stimulation and accumbal dopamine release is suppressed in ghrelin knockout mice

被引:68
|
作者
Jerlhag, Elisabet [1 ]
Landgren, Sara [1 ]
Egecioglu, Emil [2 ]
Dickson, Suzanne L. [2 ]
Engel, Jorgen A. [1 ]
机构
[1] Univ Gothenburg, Sahlgrenska Acad, Pharmacol Sect, Inst Neurosci & Physiol, Gothenburg, Sweden
[2] Univ Gothenburg, Sahlgrenska Acad, Sect Physiol Endocrinol, Inst Neurosci & Physiol, Gothenburg, Sweden
基金
瑞典研究理事会;
关键词
Ghrelin; Dopamine; Appetite; Hedonic; Reward; Ethanol; NICOTINIC ACETYLCHOLINE-RECEPTORS; CONDITIONED PLACE PREFERENCE; FOOD-INTAKE; PLASMA; ETHANOL; RATS; ASSOCIATION; CONSUMPTION; ACTIVATION; DEPENDENCE;
D O I
10.1016/j.alcohol.2010.10.002
中图分类号
R194 [卫生标准、卫生检查、医药管理];
学科分类号
摘要
Ghrelin, the first endogenous ligand for the type IA growth hormone secretagogue receptor (GHS-R1A), plays a role in energy balance, feeding behavior, and reward. Previously, we showed that pharmacologic and genetic suppression of the GHS-R1A attenuates the alcohol-induced stimulation, accumbal dopamine release, and conditioned place preference as well as alcohol consumption in mice, implying that the GHS-R1A is required for alcohol reward. The present study further elucidates the role of ghrelin for alcohol-induced dopamine release in nucleus accumbens and locomotor stimulation by means of ghrelin knockout mice. We found that the ability of alcohol to increase accumbal dopamine release in wild-type mice is not observed in ghrelin knockout mice. Furthermore, alcohol induced a locomotor stimulation in the wild-type mice and ghrelin knockout mice; however, the locomotor stimulation in homozygote mice was significantly lower than in the wild-type mice. The present series of experiments suggest that endogenous ghrelin may be required for the ability of alcohol to activate the mesolimbic dopamine system. (C) 2011 Elsevier Inc. All rights reserved.
引用
收藏
页码:341 / 347
页数:7
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