Fetal Alcohol Syndrome Research Today is a free monthly online journal that collates and summarizes the latest research about Fetal Alcohol Syndrome, including details on pregnancy, birth defects, causes, symptoms, treatment.

Single alcohol exposure in early life damages hippocampal stem/progenitor cells and reduces adult neurogenesis.

Ieraci A, Herrera DG

Department of Psychiatry, Weill Medical College of Cornell University, 1300 York Avenue, Box 244, New York, NY 10021, USA.

Alcohol exposure during pregnancy may cause fetal alcohol syndrome (FAS), characterized by impaired cognitive functions. Neurogenesis occurs in the adult hippocampus and is functionally associated with learning, memory, and mood disorders. However, whether early postnatal exposure to alcohol impairs neurogenesis and through which mechanisms it occurs is poorly understood. Here, we report that a single episode of alcohol exposure in postnatal day 7 (P7) decreases neurogenesis in the adult hippocampus. Furthermore, we demonstrate a co-localization of glial fibrillar acidic protein, nestin, and vimentin with activated caspase-3 12 h after ethanol treatment. Finally, we show that the number of primary neurospheres derived from the hippocampi of alcohol-exposed mice is reduced compared to controls. These findings suggest that alcohol exposure in postnatal mice reduces the pool of neural stem/progenitor cells in the DG, and subsequently results in a decrease of adult neurogenesis. This may explain certain aspects of impaired hippocampal functions in FAS.

Published 22 May 2007 in Neurobiol Dis, 26(3): 597-605.
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