and thus influences the onset and/or the severity of cognitive decline in various tasks, including spatial, decision-making and working memory processes (19–23). Further, sustained, high local concentration of glucocorticoids is responsible for long-lasting cognitive impairments occurring several weeks after the cessation of alcohol in rodents (24, 25) and abstinent patients (26, 27). As to how elevation of glucocorticoids might be implicated in the enduring cellular, molecular, and behavioral changes, it has been suggested that neuroadaptation induced by alcohol exposure involves the dysregulation of numerous signaling cascades, leading to long-term changes in transcriptional profiles of genes, through the actions of transcription factors such as [cAMP response element-binding protein (CREB)] and chromatin remodeling due to modifications of the posttranslational properties of histone proteins [for review, see Ref. (28)]. In the following, we provide an overview of how transcriptional and histone acetylation changes in the PFC, the HPC, and the AMG play a central role in the glucocorticoid-dependent neuroadaptation and behavioral deficits that occur during acute and chronic alcohol exposure. While this review focuses on aspects of how spatial and temporal changes in histone acetylation drive alcohol-induced alterations in neural plasticity and behavior, it should be emphasized that other histone modifications marks, such
