Multiple studies employing rodent models have investigated the impact of alcohol dependence on prefrontal cognitive capacity. Growing evidence suggests that the rodent medial prefrontal cortex (mPFC) likely represents a functional homolog of the human medial and dorsolateral PFC (109). Reports using various rodent models of alcohol dependence [including chronic intermittent ethanol vapor exposure (CIE), liquid diet, two bottle choice; for paradigm overviews, see Ref. (110)] have found behavioral inflexibility (111), impaired extinction (112), impaired set-shifting (113), and impaired working memory (114, 115), all tasks which require a fully functioning PFC. Further, two of these studies (112, 113) linked the disruption in frontal cortical function to alcohol-induced dysregulation of the N-methyl-d-aspartate glutamatergic receptor (GluN) system. Two studies have investigated PFC functions into periods of abstinence following chronic ethanol exposure via CIE (10 days abstinence; (116)), or liquid diet (6 weeks abstinence; (114)). Interestingly, at 10 days into abstinence there is a lack of impairment in cognitive flexibility while at 6 weeks into abstinence there were severe impairments in working memory. Furthermore, investigation of anxiety-like behavior, 6 weeks into abstinence, demonstrated a
