Moderate fetal alcohol exposure impairs neurogenic capacity of murine neural stem cells isolated from the adult subventricular zone.
Moderate fetal alcohol exposure impairs neurogenic capacity of murine neural stem cells isolated from the adult subventricular zone.
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DOI：
10.1016/j.expneurol.2011.03.007
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发表时间：
2011-06
影响因子：
5.3
通讯作者：
Cunningham, Lee Anna
中科院分区：
文献类型：
--
作者：
Roitbak, Tamara;Thomas, Kelsey;Martin, Ashleigh;Allan, Andrea;Cunningham, Lee Anna
关键词：
接触酒精会导致一系列神经系统症状，从高剂量接触导致的严重智力迟钝到低至中等剂量引起的微妙认知和神经精神症状。我们和其他研究人员已经证明，在整个妊娠期暴露于中等水平的酒精会导致成年海马神经发生受损，尽管这种情况发生的机制尚不清楚。为了开始区分细胞内在的微环境的贡献受损的成年神经发生，我们分离神经干祖细胞（NSPCs）从成年SVZ的小鼠暴露于中等水平的酒精在整个妊娠期。我们发现，从胎儿酒精暴露（FAE）小鼠分离的NSPCs显示减少神经球形成的文化，通过连续传代神经球测定评估，并减少神经元分化生长因子撤出。这些研究表明，妊娠期酒精暴露导致长期持续的NSPC内在失调，这可能是体内神经源性缺陷的基础。
Gestational alcohol exposure leads to a spectrum of neurological symptoms which range from severe mental retardation caused by high dose exposure, to subtle cognitive and neuropsychiatric symptoms caused by low-to-moderate doses. We and other investigators have demonstrated that exposure to moderate levels of alcohol throughout gestation leads to impaired neurogenesis in the adult hippocampus, although the mechanisms by which this occurs are not known. To begin to distinguish cell-intrinsic from microenvironmental contributions to impaired adult neurogenesis, we isolated neural stem progenitor cells (NSPCs) from the adult SVZ of mice exposed to moderate levels of alcohol throughout gestation. We found that NSPCs isolated from fetal alcohol exposed (FAE) mice displayed reduced neurosphere formation in culture, as assessed by a serial passage neurosphere assay, and reduced neuronal differentiation upon growth factor withdrawal. These studies suggest that gestational alcohol exposure leads to long-lasting NSPC-intrinsic dysregulation, which may underlie in vivo neurogenic deficits.
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