中国科技核心期刊
CN:31-1600/Q
ISSN:1004-0374
“健康与疾病的免疫”国际学术研讨会通知      关于有网站冒充本刊网站的声明
《生命科学》 2008, 20(1): 111-
酒精诱导突触发生期神经元凋亡的分子机理
刘 莹,骆 嘉,柯尊记*
(中国科学院上海生命科学研究院营养科学研究所,上海 200031)
摘 要: 在突触发生时期,酒精诱导的神经元凋亡可能是胎儿酒精综合征产生的原因之一。酒精可能通过增加自由基的产生,影响神经递质受体的功能、干扰神经营养因子信号通路、激活内源性的细胞凋亡信号途径等分子机制,促进发育过程中的神经元凋亡。酒精影响发育的另一个重要机制是抑制蛋白质合成。新近的研究显示,双链RNA激活的蛋白激酶介导酒精引起的蛋白翻译受阻和神经元死亡。
关键词:胎儿酒精综合征;酒精;神经元;凋亡
中图分类号:R714.5; R442.8; O623.411  文献标识码:A
 
The molecular mechanism of ethanol-induced neuronal apoptosis during synaptogenesis
LIU Ying, LUO Jia, KE Zun-ji*
(Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences , Shanghai 200031, China)
Abstract: Ethanol-induced neuronal apoptosis during the synaptogenesis of the brain plays a key role in the mental and behavioral deficits observed in fetal alcohol syndrome. Increasing evidences suggest that ethanol may cause neurodegeneration by increasing free radical production, interfering with the action of some neurotransmitter functions or neurotrophic actions, and activating intrinsic apoptotic signaling pathway. Another important mechanism involves inhibiting protein synthesis, a recent study shows that the double-stranded RNA activated protein kinase (PKR) mediates ethanol-induced protein synthesis inhibition and neuronal death.
Key words: fetal alcohol syndrome; ethanol; neuron; apoptosis
 
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