Loss of RAB-3/A in Caenorhabditis elegans and the mouse affects behavioral response to ethanol
Loss of RAB-3/A in Caenorhabditis elegans and the mouse affects behavioral response to ethanol
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DOI：
10.1111/j.1601-183x.2008.00404.x
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发表时间：
2008-08-01
影响因子：
2.5
通讯作者：
McIntire, S. L.
中科院分区：
文献类型：
--
作者：
Kapfhamer, D.;Bettinger, J. C.;McIntire, S. L.
乙醇诱导行为变化的机制尚不清楚。在这里，我们表明，秀丽隐杆线虫的突触囊泡相关的RAB-3蛋白和其鸟苷三磷酸交换因子AEX-3的功能丧失突变赋予抵抗急性运动乙醇的影响。类似地，缺乏Rab 3A的一个或两个拷贝的小鼠对乙醇的共济失调和镇静作用具有抗性，Rab 3A单倍不足增加了自愿的乙醇消耗。这些数据表明RAB-3-/RAB 3A调节的神经递质释放在乙醇相关行为中的保守作用。
The mechanisms by which ethanol induces changes in behavior are not well understood. Here, we show that Caenorhabditis elegans loss-of-function mutations in the synaptic vesicle-associated RAB-3 protein and its guanosine triphosphate exchange factor AEX-3 confer resistance to the acute locomotor effects of ethanol. Similarly, mice lacking one or both copies of Rab3A are resistant to the ataxic and sedative effects of ethanol, and Rab3A haploinsufficiency increases voluntary ethanol consumption. These data suggest a conserved role of RAB-3-/RAB3A-regulated neurotransmitter release in ethanol-related behaviors.