Adolescent alcohol use in human populations dramatically increases the likelihood of adult alcohol use disorder. This adolescent vulnerability is recapitulated in preclinical models which provide important opportunities to understand basic neurobiological mechanisms. We provide here an overview of GABAergic and glutamatergic neurotransmission and our current understanding of the sensitivity of these systems to adolescent ethanol exposure. As a whole, the preclinical literature suggests that adolescent vulnerability may be directly related to region-specific neurobiological processes that continue to develop during adolescence. These processes include the activity of intrinsic circuits within diverse brain regions (primarily represented by GABAergic neurotransmission) and activity-dependent regulation of synaptic strength at glutamatergic synapses. Furthermore, GABAergic and glutamatergic neurotransmission within regions/circuits that regulate cognitive function, emotion, and their integration appears to be the most vulnerable to adolescent ethanol exposure. Finally, using documented behavioral differences between adolescents and adults with respect to acute ethanol, we highlight additional circuits and regions for future study.
Keywords: AMPAR; GABAA; NMDAR.