The goal of this review was to provide initial evidence in support of the proposal that the cognitive recovery of the hippocampus and the PFC following abstinence from long-term alcohol abuse occur at different rates, potentially due to their difference in cellular composition and neurogenic functionality. For example, clinical evidence supports recovery of certain PFC-dependent tasks in times of abstinence from alcohol at different rates compared with hippocampal-dependent tasks. Preclinical findings in animal models of alcohol exposure support the clinical observation; mechanistic studies support that this temporally differential rescue of PFC-dependent tasks is potentially due to the neurogenic deficits in the hippocampus during abstinence, such that the birth of new neurons during periods of negative affect result in the persistence of the hippocampal-specific cognitive disparities.
