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中文摘要：
急性酒精中毒可引起中枢神经系统广泛的抑制,甚至造成休克。慢性酒精中毒可造成中枢神经系统损伤,Wernicke,s综合征和Korsakoff‘s是其常见表现。妊娠期酒精暴露可产生胎儿酒精系列紊乱。中枢损伤表现为大脑皮质和海马神经细胞丧失和神经细胞凋亡,大脑皮质和海马树突棘数量减少,树突棘变长;突触数量明显减少,突触的超微结构也发生改变,突触小泡数量减少,突触间隙变窄,甚至模糊不清。氧化应激相关蛋白表达增多,胰岛素抵抗指数增加。视网膜损害尤为突出,可致神经干细胞增殖、细胞凋亡,视网膜片层化结构紊乱等。酒精中毒机制复杂,有受体途径、离子通道途径、氧化应激途径等。最近,神经酰胺通路参与了酒精的毒理学机制引起了广泛关注,神经酰胺可能作为第二信使调节酒精诱导的细胞凋亡、增殖和氧化应激反应。
英文摘要：
Acute alcohol intoxication can suppress the actions of central nervous system （CNS）, even causes shock. Chronic alcohol intoxication can induce the damages in CNS, and Wernicke, s syndrome and Korsakoff＇s syndrome are their common manifestation. Prenatal alcohol exposure is the main cause of feta alcohol spectrum disorder （FASD）, and the following is the CNS damages in FASD： O neurons＇ loss and neuroapoptosis in cortex and hippocampus; （~） the dendritic spines decrease and their increase in cortical and hippocampal pyramidal cells; （~） ultrastructural alterations of synapses, such as the synapses loss, narrow synaptic cleft and synaptic vesicles decrease; （~） the expression increase of oxidative-stress protein and increase of insulin resistance; 0 retina is specifically sensitive to alcohol exposure, prenatal alcohol exposure can cause neural proliferation, neuroapoptosis and lamination disorder. The mechanism of alcohol intoxication is complicate. The receptors, ion channels and oxidative-stress are involved in the mechanism. Recently, the ceramide pathway is reported to participate in the intoxicative mechanism. As a second message signal, ceramide regulates the alcohol inducing neuroproliferation, neuroapoptosis and oxidative stress.
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