Alcohol is widely known to acutely alter cortical function by modulating inhibitory and excitatory receptor function on neuronal processes (8–10). By repressing excitatory transmission (8, 11–15) and concurrently enhancing inhibitory transmission (16–21), alcohol acutely acts as a systemic depressant. Over repeated, chronic exposures, neuronal transmission achieves a homeostatic state in the presence of alcohol (22), and cognition can resemble that of non-dependent function. However, during periods of abstinence when alcohol is absent from the system for extended phases, effectively disrupting the previously described modified homeostasis, cognitive function is significantly impaired (due to the absence of alcohol as critical modulating factor), and these cognitive impairments persist for some time. Interestingly, these cognitive perturbations, in some instances, do recover to or near pre-dependency levels. What follows is a description and synthesis of how alcohol modulates PFC and hippocampal function, what changes occur as occasional alcohol consumption becomes chronic consumption, and what cognitive impairments are present during acute withdrawal.
