Alcohol Use Disorder (AUD) is a chronic brain disease with major health and societal concerns resulting
in more deaths than any other type substance misuse. Of all the forms of alcohol misuse, binge drinking is the
most common, costly, and deadly pattern of excessive alcohol use. Addressing this major public health problem
requires a better understanding of the underlying neurobiology of binge drinking. One region of particular
interest for binge-drinking is the prelimbic cortex (PL). We have previously shown that excitatory and inhibitory
signaling in the PL is altered following a variety of models of ethanol exposure. In addition, our preliminary data
indicates that somatostatin neurons in the PL are involved in alcohol binge drinking in both sexes. This is
particularly novel as it represents a promising neuronal population capable of reducing binge drinking behavior.
Our project will (1) investigate how PL somatostatin neurons interact with other neurons (synaptic connectivity
and signaling), and (2) what role they play in binge drinking (chemogenetic activation and inhibition). Taken
together, these experiments will assess the hypothesis that somatostatin neurons in the PL are a promising
therapeutic target for alcohol use disorder, and binge drinking in particular.