Post-traumatic stress disorder (PTSD) and alcohol use disorder (AUD) have a high rate of comorbidity. While this comorbidity is well documented, its neural correlates are still poorly understood. Recent studies have shown that anxiety disorders and AUD are similarly characterized by altered amygdalar structure and activity but less is known about the specific circuits within the amygdala that promote drinking. The intercalated cells of the amygdala (ITC) are GABAergic interneurons situated around the basolateral amygdala (BLA). ITCs are known to regulate fear behaviors, such as extinction, that are relevant to PTSD, however, their role in alcohol use has not been assessed. In the current study, we investigated the effect of inhibiting ITCs on ethanol (EtOH) consumption. To this end, we used a two-bottle choice, limited access drinking in the dark paradigm to assess binge-like EtOH consumption and preference. Expression of the viral vector pAAV-hSyn-DIO-ha-Hm4d(gi)-ires-Mcitrine (Addgene) was targeted to ITC cells via injection into male and female FoxP2-Cre mice. Mice expressing hM4Di or eGFP drank 15% EtOH vs. water for 2 h over 15 sessions. On sessions 2, 5, 9, and 10 mice received injections of either the DREADD receptor ligand clozapine-n-oxide (CNO, 1 mg/kg i.p.) or vehicle 15 min before the commencement of drinking. In the final week, mice received injections of CNO or VEH before drinking ethanol adulterated with quinine. Our research is ongoing but indicates that inhibition of ITC neurons within the amygdala had no impact on alcohol consumption or preference for both sexes. Future studies will also explore whether early life stress exposure alters the relationship between ITC cell activity and alcohol drinking.
Author(s): Natalie Shand, Psychology Major
Advisor(s): Anna Radke, Department of Psychology
Thomas Perry, Department of Psychology
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