Ieraci Alessandro, Herrera Daniel G
Department of Psychiatry, Weill Medical College of Cornell University, 1300 York Avenue, Box 244, New York, NY 10021, USA.
Neurobiol Dis. 2007 Jun;26(3):597-605. doi: 10.1016/j.nbd.2007.02.011. Epub 2007 Mar 28.
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.
孕期酒精暴露可能导致胎儿酒精综合征（FAS），其特征为认知功能受损。成体海马中会发生神经发生，且在功能上与学习、记忆及情绪障碍相关。然而，出生后早期酒精暴露是否会损害神经发生以及通过何种机制发生，目前尚不清楚。在此，我们报告出生后第7天（P7）单次酒精暴露会减少成体海马中的神经发生。此外，我们证明乙醇处理12小时后，胶质纤维酸性蛋白、巢蛋白和波形蛋白与活化的半胱天冬酶-3共定位。最后，我们表明与对照组相比，酒精暴露小鼠海马来源的原代神经球数量减少。这些发现表明，出生后小鼠酒精暴露会减少齿状回中神经干/祖细胞池，随后导致成体神经发生减少。这可能解释了FAS中海马功能受损的某些方面。
