Glia and fetal alcohol syndrome

Glia and fetal alcohol syndrome
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DOI:
10.1016/s0161-813x(01)00037-7
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发表时间:
2001-10-01
期刊:
影响因子:
3.4
通讯作者:
Renau-Piqueras, J
Renau-Piqueras, J
中科院分区:
医学3区
文献类型:
--
作者:
Guerri, C;Pascual, M;Renau-Piqueras, J

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神经胶质细胞及其与神经元的相互作用在神经系统和成人大脑的个体发育过程中起着至关重要的作用。怀孕期间饮酒会导致智力迟钝、神经行为障碍以及胎儿酒精综合征(FAS)。临床和实验证据表明,子宫内酒精暴露会导致神经胶质发生和神经胶质-神经元相互作用中的结构和连接异常,这表明神经胶质细胞在酒精诱导的发育性脑异常中可能起作用。体内研究表明,乙醇在神经元和放射状胶质细胞的迁移以及星形胶质细胞的形成和髓鞘发育中具有相关的改变。在原代培养的星形胶质细胞中,乙醇被发现(1)损害细胞生长和分化,(2)降低胶质纤维酸性蛋白或GFAP(星形胶质细胞标志物)的水平及其基因表达,(3)干扰营养因子的刺激作用,影响它们的释放和受体表达。证据还表明,乙醇影响细胞内蛋白质运输,这可能介导乙醇对星形胶质细胞的某些作用。这些发现表明,神经胶质细胞是大脑发育过程中乙醇毒性的靶点,可能是子宫酒精暴露和FAS后观察到的神经发育异常的基础。(C) 2001爱思唯尔科学公司版权所有。
Glial cells and their interactions with neurons play vital roles during the ontogeny of the nervous system and in the adult brain. Alcohol intake during pregnancy can cause mental retardation and neurobehavioral disorders as well as fetal alcohol syndrome (FAS). Clinical and experimental evidence indicate that in utero alcohol exposure induces structural and junctional abnormalities in gliogenesis and in glial-neuronal interactions, suggesting a potential role of glial cells on ethanol-induced developmental brain abnormalities. In vivo studies have shown ethanol-associated alterations in the migration of neurons and radial glial as well as in astrogliogenesis and myelin development. In astrocytes in primary culture, ethanol has been found to (1) impair cell growth and differentiation, (2) decrease the levels of glial fibrillary acidic protein or GFAP (an astrocyte marker) and its gene expression and (3) interfere with the stimulatory effect of trophic factors affecting their release and receptor expression. Evidence also suggests that ethanol affects intracellular protein trafficking, which may mediate some effects of ethanol on astroglial cells. These findings suggest that glial cells are target of ethanol toxicity during brain development and may underlie the neurodevelopmental abnormalities observed after in utero alcohol exposure and in FAS. (C) 2001 Elsevier Science Inc. All rights reserved.