Enhanced and delayed stress-induced alcohol drinking in mice lacking functional CRH1 receptors
Enhanced and delayed stress-induced alcohol drinking in mice lacking functional CRH1 receptors
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DOI：
10.1126/science.1069836
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发表时间：
2002-05-03
期刊：
影响因子：
56.9
通讯作者：
Spanagel, R
中科院分区：
文献类型：
--
作者：
Sillaber, I;Rammes, G;Spanagel, R
压力和饮酒之间存在关联。我们发现促肾上腺皮质激素释放激素（CRH）系统介导内分泌和对压力的行为反应，在控制长期饮酒中发挥着作用。在缺乏功能性 CRH1 受体的小鼠中，压力会导致酒精摄入量增加并逐渐增加。反复压力对饮酒行为的影响会延迟出现并持续一生。它与 N-甲基-D-天冬氨酸受体亚基 NR2B 的上调有关。 CRH1受体基因的改变和NR2B亚基的适应性变化可能构成压力诱发饮酒和酒精中毒的遗传危险因素。
There is a relation between stress and alcohol drinking. We show that the corticotropin-releasing hormone (CRH) system that mediates endocrine and behavioral responses to stress plays a role in the control of long-term alcohol drinking. In mice lacking a functional CRH1 receptor, stress leads to enhanced and progressively increasing alcohol intake. The effect of repeated stress on alcohol drinking behavior appeared with a delay and persisted throughout life. It was associated with an up-regulation of the N-methyl-D-aspartate receptor subunit NR2B. Alterations in the CRH1 receptor gene and adaptional changes in NR2B subunits may constitute a genetic risk factor for stress-induced alcohol drinking and alcoholism.