of data showing that elevated glucocorticoid levels, via either systemic injection of corticosterone or local infusion of the GRs agonist RU 28362 into the medial PFC shortly before testing, similarly impair working memory (55), while the GRs antagonist RU 38486 infused into the PFC can restore stress-induced deficits in executive function (58). Collectively, these data support the view that long-term adaptive behavioral effects of chronic alcohol exposure are mediated in large part through long-lasting glucocorticoid dysregulation within the PFC circuitry.
