A wealth of evidence from clinical findings demonstrates that acute alcohol exposures can inhibit cognitive capacities. Interestingly, it is primarily following withdrawal from chronic alcohol exposure that individuals experience persisting, severe cognitive impairments. As eloquently described in Oscar-Berman et al. (104), studies involving human subjects and drugs of abuse are often rife with complicating and confounding factors, including family history, genetic predisposition, and past life events and experience, much of which cannot be controlled for. While clinical studies are limited to observational investigations into the deleterious cortical adaptations subsequent to chronic alcohol exposure, preclinical models have been successful at informing and elaborating our understanding of the cellular and molecular changes, which may explain the mechanisms underlying cognitive disparities in abstinent alcohol-dependent subjects. Further, preclinical models of alcohol dependence have generated evidence suggesting that the distinct cellular compositions of the PFC and the hippocampus may be the basis for the differential cognitive recovery in these regions in abstinent individuals. Therefore, the following sections will discuss preclinical models of alcohol addiction and dependence with specific focus on cognitive impairments dependent on the PFC and hippocampus and will elucidate the associated cellular and molecular changes in these regions.
