Effects of adolescent binge ethanol exposure on striatal parvalbumin

Binge drinking is the most common, costly, and deadly pattern of excessive alcohol use in the United States. About 27% of people ages 18 or older reported binge drinking in the past month. Studies show that binge drinking among adolescents may lead to alcohol-use disorders later in life. Animal models of binge drinking show that adolescent intermittent ethanol (AIE) exposure in rodents can alter synaptic physiology, sensitivity to alcohol, and behavior and cause the adolescent-like phenotype to persist into adulthood. Striatal subregions play distinct roles in the integration of social information and coordinated movement, but alcohol exposure has been shown to cause dysfunctional connectivity and deficits in neuronal activity, inhibiting striatal output. A decrease of parvalbumin (PV) neurons in various brain regions has been associated with deficits in cognitive control and decision-making, most likely because PV interneurons regulate the excitatory/inhibitory balance that drive appropriate behavioral responses. Some studies have investigated the effect of perinatal alcohol exposure on PV in various brain regions, however, the effect of binge level alcohol exposure on PV, specifically in the striatum, is unknown. The present study is the first to test AIE-induced effects on striatal PV. We hypothesized that AIE-induced reductions in PV interneuron markers are associated with AIE reductions in behavioral flexibility and functional connectivity. However, using immunohistochemistry (IHC) and fluorescent microscopy, we report here that AIE does not significantly alter striatal PV+IR interneurons (p > 0.05) and PV interneurons do not play a significant role in the genesis of the behavioral deficits associated with each striatal subregion.Bachelor of Scienc