The Impact of Adolescent Ethanol Drinking on Astrocyte Genes Regulating Glutamatergic Transmission in the Adult Prefrontal Cortex

Authors: Camryn McLean, Andrea Liss, Florence Varodayan

Field of Study: Psychology

Program Affiliation: Undergraduate Research Award, Varodayan Neuroscience Lab

Faculty Mentors: Florence Varodayan

Easel: 4

Timeslot: Morning

Abstract: Drinking during adolescence increases the risk of alcohol use disorder (AUD), affecting millions of Americans. The medial prefrontal cortex (mPFC), responsible for executive functioning, does not fully mature until early adulthood, making it vulnerable to alcohol-induced damage. Chronic alcohol exposure disrupts mPFC function, though underlying cellular mechanisms remain unclear. Astrocytes regulate synaptic communication by controlling glutamate, an excitatory neurotransmitter implicated in drug dependence. Individuals with AUD often exhibit elevated glutamate levels during withdrawal. Previous findings from this laboratory show increased glutamate transporter-1 (GLT-1) and cystine–glutamate antiporter (xCT) mRNA in the mPFC after twelve days of withdrawal from adult ethanol exposure, suggesting a compensatory response. However, effects of adolescent exposure remain unknown. Adolescent mice underwent intermittent ethanol exposure (P30–60); mPFC tissue was collected in adulthood (P90–94) and analyzed via RT-PCR. It is hypothesized this exposure will increase GLT-1 and xCT expression, reflecting compensatory neuroadaptation and identifying potential targets for AUD treatment.