Abstract
The chances of developing alcoholism throughout one's life are determined by a genetic predisposition and an individual's reaction to lifetime events, such a stress. The corticotropin-releasing hormone (CRH) system regulates endocrine responses to stress and mediates stress-related behavior. To better understand the molecular and cellular mechanism underlying stress-induced alcohol drinking Sillaber et al. created knockout mice lacking CRH1 receptors. Crhr1 −/− mice did not differ from wild-type mice in their basal alcohol intake and preference. However, after repeated stress episodes, the knockout mice gradually increased their alcohol consumption and kept it elevated for the rest of their life. This change in drinking behavior was accompanied by enhanced protein levels of the NR2B subunit of the N-methyl-D-aspartate receptor. I. Sillaber, G. Rammes, S. Zimmermann, B. Mahal, W. Zieglgänsberger, W. Wurst, F. Holsboer, R. Spanagel, Enhanced and delayed stress-induced alcohol drinking in mice lacking functional CRH1 receptors. Science 296 , 931-933 (2002). [Abstract] [Full Text]
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