Alcohol Use Disorder (AUD) is a complex psychiatric disorder with large societal and personal strain, involving
many brain regions and cell types. Few effective treatments exist that specifically target the prevention of binge
drinking. Understanding the underlying neurobiology of binge drinking is essential for preventing and treating
this major public health problem. Ongoing work in our lab seeks to understand how somatostatin (SST)
expressing GABAergic neurons in the prelimbic (PL) cortex, which have long been implicated in other
neuropsychiatric disorders as an anti-depressive, resilience-conferring population of peptidergic neurons, may
function as a therapeutic target for AUD. The overarching goal of this proposal is to understand how
SST peptide signaling contributes to PL circuitry function, and how these pathways are
modulated by binge alcohol consumption. Using a combination of electrophysiology, circuit mapping,
fiber photometry, and behavior, we will explore three complementary but non-overlapping aims: we will
demonstrate how SST modulates prelimbic pyramidal neurons, the specific outputs modulated by SST, and the
overall behavioral phenotype of SST administration to the PL cortex. We will conduct these experiments during
control conditions and in the context of binge drinking.
Taken together, these experiments will determine the overall role of SST peptide effects on pathway-specific
circuits of the PL cortex. In addition, we will establish the in vivo effects of SST peptide on alcohol consumption
and anxiety-like behaviors, providing an overall mechanistic and functional characterization of SST in the PL
cortex. These results will build upon our previous findings to elucidate the precise role of the SST peptide.
Importantly, we expect these results to have the potential to inform new treatment targets for AUD.