Biological studies on alcohol-induced neuronal damage.
Biological studies on alcohol-induced neuronal damage.
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DOI：
10.4306/pi.2008.5.1.21
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发表时间：
2008-03
影响因子：
2.7
通讯作者：
Saito T
中科院分区：
文献类型：
--
作者：
Tateno M;Saito T
酒精是一种众所周知的细胞毒性剂，可引起各种神经元损伤。尽管发表了数千项研究，但酒精诱导神经元损伤的真正机制仍不清楚。神经发生是从神经干细胞（NSC）产生神经元，并且主要发生在脑的两个区域，脑室下区和海马的齿状回。NSC是中枢神经系统中神经元、星形胶质细胞和少突胶质细胞的自我更新的多能前体细胞。最近的研究已经开始阐明神经发生在精神疾病的生物和细胞基础中的作用，并且在酒精中毒中看到的几种临床症状，如抑郁症，认知障碍，潜在的压力和脑萎缩，已经与受损的神经发生有关。大量饮酒会减少动物的神经发生，而体外研究表明，酒精暴露后新神经元的生成减少。这些发现表明，减少神经发生是重要的病理生理学酒精中毒。神经发生可分为四个阶段：增殖、迁移、分化和存活。我们对神经干细胞的体外研究表明，酒精在低于影响细胞存活的剂量下会降低神经元分化，并表明神经元限制性沉默因子或阻遏物元件1沉默转录因子（NRSF/REST）可能参与酒精诱导的神经元分化抑制。在胎儿酒精影响的动物模型中，NSC移植后行为症状改善。神经发生可能是治疗酒精相关疾病的新策略的目标。
Alcohol is a well-known cytotoxic agent which causes various kinds of neuronal damage. In spite of thousands of published studies, the true mechanism of alcohol-induced neuronal damage remains unclear. Neurogenesis is the generation of neurons from neural stem cells (NSCs) and occurs in predominantly two regions of the brain, the subventricular zone and the dentate gyrus of the hippocampus. NSCs are the self-renewing, multipotent precursor cells of neurons, astrocytes, and oligodendrocytes in the central nervous system. Recent studies have begun to illuminate the role of neurogenesis in the biological and cellular basis of psychiatric disorders and several clinical symptoms seen in alcoholism such as depression, cognitive impairment, underlying stress and brain atrophy have been linked to impaired neurogenesis. Heavy alcohol consumption decreases neurogenesis in animals, while in vitro studies have shown decreased generation of new neurons after alcohol exposure. These findings suggest that decreased neurogenesis is important in the pathophysiology of alcoholism. Neurogenesis can be divided into four stages; proliferation, migration, differentiation and survival. Our in vitro studies on NSCs showed that alcohol decreased neuronal differentiation at doses lower than those that affected cell survival and suggested that neuron-restrictive silencer factor, or repressor element-1 silencing transcription factor (NRSF/REST) could be involved in alcohol-induced inhibition of neuronal differentiation. In an animal model of fetal alcohol effects behavioral symptoms improved after NSC transplantation. Neurogenesis could be the target for new strategies to treat alcohol related disorders.
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