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CRF 1 Receptor Signaling Regulates Food and Fluid Intake in the Drinking‐in‐the‐Dark Model of Binge Alcohol Consumption
Author(s) -
Giardino William J.,
Ryabinin Andrey E.
Publication year - 2013
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/acer.12076
Subject(s) - endocrinology , medicine , receptor , blockade , knockout mouse , binge drinking , self administration , alcohol , chemistry , food intake , alcohol consumption , biochemistry
Background Several recent studies implementing the standard “drinking‐in‐the‐dark” ( DID ) model of short‐term binge‐like ethanol ( E t OH ) intake in C 57 BL /6 J mice highlighted a role for the stress‐related neuropeptide corticotropin‐releasing factor ( CRF ) and its primary binding partner, the CRF type‐1 (CRF1) receptor. Methods We evaluated the selectivity of CRF 1 involvement in binge‐like E t OH intake by interrupting CRF 1 function via pharmacological and genetic methods in a slightly modified 2‐bottle choice DID model that allowed calculation of an E t OH preference ratio. In addition to determining E t OH intake and preference, we also measured consumption of food and H 2 O during the DID period, both in the presence and absence of E t OH and sweet tastant solutions. Results Treatment with either of the CRF 1‐selective antagonists CP ‐376,395 (CP; 10 to 20 mg/kg, i.p.) or NBI ‐27914 (10 to 30 mg/kg, i.p.) decreased intake of 15% Et OH in male C 57 BL /6 J mice, but did so in the absence of a concomitant decrease in E t OH preference. These findings were replicated genetically in a CRF 1 knockout ( KO ) mouse model (also on a C 57 BL /6 J background). In contrast to effects on E t OH intake, pharmacological blockade of CRF 1 with CP increased intake of 10% sucrose, consistent with previous findings in CRF 1 KO mice. Finally, pharmacological and genetic disruption of CRF 1 activity significantly reduced feeding and/or total caloric intake in all experiments, confirming the existence of nonspecific effects. Conclusions Our findings indicate that blockade of CRF 1 receptors does not exert specific effects on E t OH intake in the DID paradigm, and that slight modifications to this procedure, as well as additional consummatory control experiments, may be useful when evaluating the selectivity of pharmacological and genetic manipulations on binge‐like E t OH intake.