Mice lacking metabotropic glutamate receptor 4 do not show the motor stimulatory effect of ethanol
Mice lacking metabotropic glutamate receptor 4 do not show the motor stimulatory effect of ethanol
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DOI：
10.1016/j.alcohol.2004.10.003
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发表时间：
2004-10-01
期刊：
影响因子：
2.3
通讯作者：
Harris, RA
中科院分区：
文献类型：
--
作者：
Blednov, YA;Walker, D;Harris, RA
III 类代谢型谷氨酸受体 (mGluR)，特别是受体 4、6、7 和 8（即 mGluR4、mGluR6、mGluR7、mGluR8），在运动的产生以及某些精神兴奋剂的行为效应中发挥着重要作用。由于乙醇的唤醒或刺激作用似乎与其奖励特性和对酗酒的遗传易感性相关的行为特征有关，因此我们通过研究乙醇在缺乏 mGluR4 的突变小鼠中的行为作用来解决 mGluR4 的作用。无效突变小鼠比野生型小鼠对新奇事物表现出更高的运动反应。乙醇（1.0-2.5 g/kg）刺激野生型小鼠的运动活动，但不刺激无效突变小鼠的运动活动。野生型和敲除菌株之间在乙醇消耗或两瓶模式偏好、乙醇诱导的急性戒断的严重程度或翻正反射丧失的持续时间方面没有显着差异。这些结果表明，mGluR4 可能在一般运动活动中发挥作用，并且还显示出介导乙醇运动刺激作用的特异性。与其他研究的结果一致，这些结果证实了乙醇诱导的运动刺激与小鼠自我给药范例中测量的乙醇消耗之间缺乏相关性。 (c) 2005 Elsevier Inc. 保留所有权利。
Group III metabotropic glutamate receptors (mGluRs), specifically receptors 4, 6, 7, and 8 (i.e., mGluR4, mGluR6, mGluR7, mGluR8), play an important role in the generation of locomotion as well as in the behavioral effects of some psychostimulants. Because the arousing or stimulant effects of ethanol seem to be relevant behavioral traits associated with its rewarding properties and genetic susceptibility to alcoholism, we addressed the role of mGluR4 by studying behavioral actions of ethanol in mutant mice lacking mGluR4. Null mutant mice showed higher motor response to novelty than did wild-type mice. Ethanol (1.0-2.5 g/kg) stimulated motor activity of wild-type mice, but not of null mutant mice. there were no significant differences between wild-type and knockout strains in ethanol consumption or preference in two-bottle paradigm, severity of ethanol-induced acute withdrawal, or duration of loss of righting reflex. These results show that mGluR4 may play a role in locomotor activity in general and also display specificity for mediation of the motor stimulant effect of ethanol. Consistent with findings of other studies, these results confirm the lack of correlation between ethanol-induced motor stimulation and consumption of ethanol measured in a self-administration paradigm in mice. (c) 2005 Elsevier Inc. All rights reserved.