Background: Adolescent intermittent ethanol (AIE) exposure causes long-term changes in the brain and behavior of adult male rodents, including persistent induction of innate immune pathways, reductions in hippocampal neurogenic and forebrain cholinergic neuronal markers, and reversal learning deficits. The current study tests the hypothesis that proinflammatory induction mediates AIE-induced (1) loss of adult neurogenesis (i.e.
View Article and Find Full Text PDFBackground: Binge ethanol exposure during adolescence reduces hippocampal neurogenesis, a reduction which persists throughout adulthood despite abstinence. This loss of neurogenesis, indicated by reduced doublecortin+ immunoreactivity (DCX+IR), is paralleled by an increase in hippocampal proinflammatory signaling cascades. As galantamine, a cholinesterase inhibitor, has anti-inflammatory actions, we tested the hypothesis that galantamine would prevent (study 1) or restore (study 2) AIE induction of proinflammatory signals within the hippocampus as well as AIE-induced loss of hippocampal neurogenesis.
View Article and Find Full Text PDFBinge drinking is common in adolescence. Rodent studies modeling adolescent binge drinking find persistent effects on the brain's physiology, including increased expression of neuroimmune genes, impaired neurogenesis, and changes in behavioral flexibility. This study used females and males to investigate the effects of adolescent intermittent ethanol (AIE) on a battery of behaviors assessing spatial navigation using a radial arm water maze, working memory using the Hebb-Williams maze, non-spatial long-term memory using novel object recognition, and dominance using a tube dominance test.
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