ABSTRACT
Alcohol use disorder (AUD) is characterized by alcohol use coupled with chronic relapse and involves brain regions including the bed nucleus of the stria terminalis (BNST). Here, we explore whether a subpopulation of BNST neurons, somatostatin (SST) expressing GABAergic neurons, play a role in an animal model of binge-like alcohol consumption, the Drinking in the Dark (DID) model. Chemogenetic activation of BNST SST neurons reduced binge alcohol consumption in female but not male SST-Cre mice, while inhibition of these neurons in the same mice had no effect. In addition, chemogenetic activation of these neurons did not cause apparent changes in models of anxiety-like behavior in either sex. Basal SST cell counts and intrinsic excitability of SST neurons were compared to attempt to understand sex differences in DREADD-induced changes in drinking, and while males had a greater number of BNST SST neurons, this effect went away when normalizing for total BNST volume. Together, these results suggest SST neurons in the BNST should be further explored as a potential neuronal subtype modulated by AUD, and for their therapeutic potential.
HIGHLIGHTS
Chemogenetic activation of BNST SST neurons reduces binge drinking in female but not male mice
Chemogenetic activation of these neurons has no effect on anxiety-like behavior in either sex
Electrophysiology revealed no clear sex differences in intrinsic excitability BNST SST neurons between males and females
Imaging revealed males had greater overall BNST SST cell numbers than females, but this effect could be explained by normalizing for total BNST volume
Competing Interest Statement
The authors have declared no competing interest.
