Corticotropin-releasing factor receptor antagonism in the central amygdala reduces binge-like ethanol intake of CRF-Cre Transgenic mice (2016)

Undergraduates: Suzahn Ebert, Todd Thiele, Ph.D.

Faculty Advisor: Alex Marshall
Department: Biology

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Binge-like ethanol consumption is characterized by the rapid achievement of blood ethanol concentration (BEC) of ?80 mg/dl and is associated with an increased risk of ethanol dependence. Evidence of this association is based on an overlap between neurobiological mechanisms active during ethanol dependence and those activated during excessive ethanol consumption prior to dependence. One such contributor is the corticotropin-releasing factor (CRF) system. Our laboratory has shown that antagonism of CRF receptors within the central amygdala (CeA) reduces binge-like ethanol consumption. The current study was designed to extend previous research by measuring ethanol consumption following the manipulation of CRF signaling in the CeA using Cre-induced inhibitory designer receptors exclusively activated by designer drugs (DREADDs) technology. Ethanol or sucrose, consumption of which is indicative of general rewarding behavior, was administered using a 4-day procedure that mimics binge-like drinking. On the first two test days, mice received drug injections to activate the DREADDs, thereby inhibiting CRF neurons within the CeA. Statistical analysis revealed that Gi-DREADD activation in the CeA reduced ethanol consumption but had no significant effect on sucrose consumption. These data suggest that the reduced ethanol consumption during the first two cycles was not merely a general rewarding behavior but was instead specific to ethanol consumption.