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Enhanced and delayed stress-induced alcohol drinking in mice lacking functional CRH1 receptors

MPS-Authors

Sillaber,  I
Max Planck Institute of Psychiatry, Max Planck Society;

Rammes,  G
Max Planck Institute of Psychiatry, Max Planck Society;

Zimmermann,  S
Max Planck Institute of Psychiatry, Max Planck Society;

Mahal,  B
Max Planck Institute of Psychiatry, Max Planck Society;

Zieglgänsberger,  W
Max Planck Institute of Psychiatry, Max Planck Society;

Wurst,  W
Max Planck Institute of Psychiatry, Max Planck Society;

Holsboer,  F
Max Planck Institute of Psychiatry, Max Planck Society;

Spanagel,  R
Max Planck Institute of Psychiatry, Max Planck Society;

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Citation

Sillaber, I., Rammes, G., Zimmermann, S., Mahal, B., Zieglgänsberger, W., Wurst, W., et al. (2002). Enhanced and delayed stress-induced alcohol drinking in mice lacking functional CRH1 receptors. Science, 296(5569), 931-933.


Cite as: http://hdl.handle.net/11858/00-001M-0000-000E-A1E1-4
Abstract
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 alcoholis