Ethanol-induced apoptotic neurodegeneration and fetal alcohol syndrome
Ethanol-induced apoptotic neurodegeneration and fetal alcohol syndrome
复制标题
DOI：
10.1126/science.287.5455.1056
复制
发表时间：
2000-02-11
期刊：
影响因子：
56.9
通讯作者：
Olney, JW
中科院分区：
文献类型：
--
作者：
Ikonomidou, C;Bittigau, P;Olney, JW
乙醇对发育中的人类大脑的有害影响知之甚少。本文报道了乙醇通过双重机制[N-甲基-D-天冬氨酸（NMDA）谷氨酸受体的阻断和GABA受体的过度激活]起作用，在发育中的大鼠前脑中引发广泛的凋亡性神经变性。脆弱性与突触发生期相吻合，人类的突触发生期从怀孕的第六个月一直持续到出生后的几年。在此期间，短暂的乙醇暴露可以从发育中的大脑中删除数百万个神经元。这可以解释与人类胎儿酒精综合征相关的脑质量减少和神经行为障碍。
The deleterious effects of ethanol an the developing human brain are poorly understood. Here it is reported that ethanol, acting by a dual mechanism [blockade of N-methyl-D-aspartate (NMDA) glutamate receptors and excessive activation of GABA, receptors], triggers widespread apoptotic neurodegeneration in the developing rat forebrain. Vulnerability coincides with the period of synaptogenesis, which in humans extends from the sixth month of gestation to several years after birth. During this period, transient ethanol exposure can delete millions of neurons from the developing brain. This can explain the reduced brain mass and neurobehavioral disturbances associated with human fetal alcohol syndrome.