Abstract

Initiation of alcohol use and subsequent binge drinking during adolescence are major risk factors for developing an alcohol use disorder later in life. Such consequential effects later in adulthood are largely preserved in animal models using adolescent ethanol exposure (AIE), with recent work demonstrating sex-dissociable effects. A lack of top-down inhibition is often prevalent in behavioral alterations following AIE. The medial prefrontal cortex (mPFC) has been highly implicated in behaviors that are altered following AIE, but the neural mechanisms through which this occurs are unknown. The present study was designed to identify the prelimbic and infralimbic cortical activated neural cell types in cFos-LacZ transgenic male and female Sprague-Dawley rats, which produce β-galactosidase as a proxy for activated neurons. We hypothesized that AIE results in dysregulation of GABA- and glutamatergic neurons in the prefrontal cortex. More specifically, AIE in males will result in a significant decrease in the activation of glutamatergic cells and an increase or no change in the number of GABAergic cells activated. Females are not predicted to have significant differences in this region. Subjects were exposed to ethanol or water via intragastric gavage on alternating days during early adolescence (P25-45). Social testing was run on day P70 after which brain tissue was collected. Brains were coronally sliced and subjected to dual-immunofluorescent staining for β-galactosidase and CamKIIalpha, a marker for glutamatergic cells. Slices were imaged and are currently being analyzed. These results will assist with further elucidating post-AIE neural contributors to alcohol use disorder.