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The CRF‐1 Receptor Antagonist, CP‐154,526, Attenuates Stress‐Induced Increases in Ethanol Consumption by BALB/cJ Mice
Author(s) -
Lowery Emily G.,
Sparrow Angela M.,
Breese George R.,
Knapp Darin J.,
Thiele Todd E.
Publication year - 2008
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.2007.00573.x
Subject(s) - ethanol , antagonist , chemistry , intraperitoneal injection , endocrinology , medicine , receptor antagonist , receptor , biochemistry
Background: Corticotropin‐releasing factor (CRF) signaling modulates neurobiological responses to stress and ethanol, and may modulate observed increases in ethanol consumption following exposure to stressful events. The current experiment was conducted to further characterize the role of CRF 1 receptor (CRF 1 R) signaling in stress‐induced increases in ethanol consumption in BALB/cJ and C57BL/6N mice. Methods: Male BALB/cJ and C57BL/6N mice were given continuous access to 8% (v/v) ethanol and water for the duration of the experiment. When a baseline of ethanol consumption was established, animals were exposed to 5 minutes of forced swim stress on each of 5 consecutive days. Thirty minutes before each forced swim session, animals were given an intraperitoneal injection of a 10 mg/kg dose of CP‐154,526, a selective CRF 1 R antagonist, or an equal volume of vehicle. The effect of forced swim stress exposure on consumption of a 1% (w/v) sucrose solution was also investigated in an ethanol‐naïve group of BALB/cJ mice. Results: Exposure to forced swim stress significantly increased ethanol consumption by the BALB/cJ, but not of the C57BL/6N, mice. Stress‐induced increases in ethanol consumption were delayed and became evident approximately 3 weeks after the first stressor. Additionally, forced swim stress did not cause increases of food or water intake and did not promote delayed increases of sucrose consumption. Importantly, BALB/cJ mice pretreated with the CRF 1 R antagonist showed blunted stress‐induced increases in ethanol intake, and the CRF 1 R antagonist did not influence the ethanol drinking of non‐stressed mice. Conclusions: The present results provide evidence that CRF 1 R signaling modulates the delayed increase of ethanol consumption stemming from repeated exposure to a stressful event in BALB/cJ mice.