Alcohol-induced neuroapoptosis in the fetal macaque brain.
Alcohol-induced neuroapoptosis in the fetal macaque brain.
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DOI：
10.1016/j.nbd.2010.05.025
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发表时间：
2010-10
影响因子：
6.1
通讯作者：
Olney JW
中科院分区：
文献类型：
--
作者：
Farber NB;Creeley CE;Olney JW
短期暴露于酒精的能力，导致广泛的神经细胞凋亡，在发育中的啮齿动物的大脑和随后的长期神经认知缺陷已被提出作为一种机制的神经行为缺陷的胎儿酒精谱系障碍（FASD）。目前还不清楚短暂接触酒精是否会导致灵长类动物胎儿大脑的细胞凋亡。将处于不同妊娠阶段（G105至G155）的妊娠食蟹猴暴露于酒精中8小时，然后通过剖腹产分娩胎儿，并用固定剂灌注其脑并评价细胞凋亡。与生理盐水对照组相比，乙醇暴露的大脑显示出一种神经细胞凋亡的模式，这种模式广泛存在，与婴儿啮齿动物大脑中酒精引起的神经细胞凋亡相似。观察到的细胞凋亡增加约为60倍。我们认为，酒精的致聋作用可以解释许多与人类FASD相关的神经病理学变化和长期神经精神障碍。
The ability of brief exposure to alcohol to cause widespread neuroapoptosis in the developing rodent brain and subsequent long-term neurocognitive deficits has been proposed as a mechanism underlying the neurobehavioral deficits seen in fetal alcohol spectrum disorder (FASD). It is unknown whether brief exposure to alcohol causes apoptosis in the fetal primate brain. Pregnant fasicularis macaques at various stages of gestation (G105 to G155) were exposed to alcohol for 8 hours, then the fetuses were delivered by caesarian section and their brains perfused with fixative and evaluated for apoptosis. Compared to saline control brains, the ethanol-exposed brains displayed a pattern of neuroapoptosis that was widespread and similar to that caused by alcohol in infant rodent brain. The observed increase in apoptosis was on the order of 60-fold. We propose that the apoptogenic action of alcohol could explain many of the neuropathological changes and long-term neuropsychiatric disturbances associated with human FASD.
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DOI：
10.1111/j.1530-0277.1993.tb00808.x
发表时间：
1993-06-01
影响因子：
3.2
作者：
HAMRE, KM;WEST, JR
通讯作者：
WEST, JR
影响因子：
5.1
作者：
CLARREN, SK;ASTLEY, SJ;SPELLMAN, D
通讯作者：
SPELLMAN, D
影响因子：
2.5
作者：
DOBBING, J;SANDS, J
通讯作者：
SANDS, J
影响因子：
5.7
作者：
Cattano, Davide;Young, Chainllie;Olney, John W.
通讯作者：
Olney, John W.
影响因子：
2.9
作者：
BAUERMOFFETT, C;ALTMAN, J
通讯作者：
ALTMAN, J