Ethanol-induced caspase-3 activation in the in vivo developing mouse brain
Ethanol-induced caspase-3 activation in the in vivo developing mouse brain
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DOI：
10.1006/nbdi.2001.0475
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发表时间：
2002-03-01
影响因子：
6.1
通讯作者：
Roth, KA
中科院分区：
文献类型：
--
作者：
Olney, JW;Tenkova, T;Roth, KA
最近几种方法已被描述为触发广泛的凋亡神经退行性病变在体内发育的哺乳动物大脑。这些方法包括用阻断NMDA谷氨酸受体的药物、促进GABA（A）神经传递的药物治疗，或用乙醇治疗，乙醇具有NMDA拮抗剂和GABA模拟物性质。由这些药剂中的任何一种引起的单一中毒事件足以引起遍及许多脑区域的广泛神经变性。细胞死亡过程在几个小时内从早期到晚期迅速发生。随着神经元死亡，它们变成TUNEL阳性，并且通过光镜和电镜显示出凋亡的所有经典形态学特征。在本研究中，使用免疫细胞化学方法，我们的文件，乙醇中毒的7天大的婴儿小鼠引起广泛的模式caspase-3激活对应的模式，同时发生的凋亡性神经变性。(C)2002 Elsevier Science（美国）。
Recently several methods have been described for triggering extensive apoptotic neurodegeneration in the developing in vivo mammalian brain. These methods include treatment with drugs that block NMDA glutamate receptors, drugs that promote GABA(A) neurotransmission, or treatment with ethanol, which has both NMDA antagonist and GABAmimetic properties. A single intoxication episode induced by any of these agents is sufficient to cause widespread neurodegeneration throughout many brain regions. The cell death process transpires rapidly from early to late stages within several hours. As the neurons die, they become TUNEL positive and show, by both light and electron microscopy, all of the classical morphological characteristics of apoptosis. In the present study, using immunocytochemical methods, we document that ethanol intoxication of 7-day-old infant mice causes a widespread pattern of caspase-3 activation corresponding to the pattern of apoptotic neurodegeneration that is occurring simultaneously. (C) 2002 Elsevier Science (USA).