Effects of Ethanol on the Cerebellum: Advances and Prospects.
Effects of Ethanol on the Cerebellum: Advances and Prospects.
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DOI：
10.1007/s12311-015-0674-8
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发表时间：
2015-08
期刊：
影响因子：
3.5
通讯作者：
Luo, Jia
中科院分区：
文献类型：
--
作者：
Luo, Jia
酗酒会导致小脑功能障碍，小脑性共济失调是酗酒者的常见特征。发育过程中接触酒精也会影响小脑。患有胎儿酒精谱系障碍 (FASD) 的儿童表现出许多与小脑缺陷特别相关的症状。然而，其细胞和分子机制尚不清楚。本期特刊讨论了酒精引起的小脑缺陷机制研究的最新进展。 GABAA 受体依赖性神经传递的改变是乙醇引起的小脑功能障碍的潜在机制。最近的进展表明，乙醇诱导的 GABA 释放增加不仅存在于浦肯野细胞 (PC) 中，而且存在于分子层中间神经元和颗粒细胞中。乙醇被证明会破坏苔藓纤维-颗粒细胞-高尔基细胞（MGG）突触位点和颗粒细胞平行纤维-PC（GPP）突触位点的分子活动，这可能是乙醇诱导的小脑共济失调的原因。衰老和乙醇可能会影响PC树突的平滑内质网（SER）并导致树突退化。乙醇戒断会导致小脑线粒体损伤和基因异常修饰。这些事件之间的相互作用可能导致神经元变性，从而导致运动缺陷。乙醇会激活双链 RNA (dsRNA) 激活蛋白激酶 (PKR)，PKR 激活涉及乙醇诱导的小脑发育中的神经炎症和神经毒性。乙醇会在 PC 丢失后改变小脑回路的发育，这可能会导致接收小脑输入的其他大脑区域的结构和功能发生变化。最后，评估了胆碱（一种必需营养素）对乙醇引起的小脑损伤的潜在保护作用。在接触乙醇之前给予胆碱可改善乙醇引起的小脑功能障碍。
Alcohol abuse causes cerebellar dysfunction and cerebellar ataxia is a common feature in alcoholics. Alcohol exposure during development also impacts the cerebellum. Children with fetal alcohol spectrum disorder (FASD) show many symptoms associated specifically with cerebellar deficits. However, the cellular and molecular mechanisms are unclear. This special issue discusses the most recent advances in the study of mechanisms underlying alcohol-induced cerebellar deficits. The alteration in GABAA receptor-dependent neurotransmission is a potential mechanism for ethanol-induced cerebellar dysfunction. Recent advances indicate ethanol-induced increases in GABA release are not only in Purkinje cells (PCs), but also in molecular layer interneurons and granule cells. Ethanol is shown to disrupt the molecular events at the mossy fiber – granule cell – Golgi cell (MGG) synaptic site and granule cell parallel fibers – PCs (GPP) synaptic site, which may be responsible for ethanol-induced cerebellar ataxia. Aging and ethanol may affect the smooth endoplasmic reticulum (SER) of PC dendrites and cause dendritic regression. Ethanol withdrawal causes mitochondrial damage and aberrant gene modifications in the cerebellum. The interaction between these events may result in neuronal degeneration, thereby contributing to motoric deficit. Ethanol activates double-stranded RNA (dsRNA)-activated protein kinase (PKR) and PKR activation is involved ethanol-induced neuroinflammation and neurotoxicity in the developing cerebellum. Ethanol alters the development of cerebellar circuitry following the loss of PCs, which could result in modifications of the structure and function of other brain regions that receive cerebellar inputs. Lastly, choline, an essential nutrient is evaluated for its potential protection against ethanol-induced cerebellar damages. Choline is shown to ameliorate ethanol-induced cerebellar dysfunction when given before ethanol exposure.
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DOI：
10.1111/j.1530-0277.2002.tb02595.x
发表时间：
2002-05-01
影响因子：
3.2
作者：
Sullivan, EV;Desmond, JE;Pfefferbaum, A
通讯作者：
Pfefferbaum, A
影响因子：
4.8
作者：
Chen, Gang;Ma, Cuiling;Luo, Jia
通讯作者：
Luo, Jia
DOI：
10.1007/s12311-015-0651-2
发表时间：
2015-08
期刊：
Cerebellum (London, England)
影响因子：
--
作者：
Light KE;Hayar AM;Pierce DR
通讯作者：
Pierce DR
影响因子：
3.5
作者：
Li, Hui;Chen, Jian;Chen, Gang
通讯作者：
Chen, Gang
影响因子：
3.8
作者：
Autti-Rämo, I;Autti, T;Valanne, L
通讯作者：
Valanne, L