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Microglia Dystrophy Following Binge-Like Alcohol Exposure in Adolescent and Adult Male Rats.
Frontiers in Neuroanatomy ( IF 2.9 ) Pub Date : 2020-08-13 , DOI: 10.3389/fnana.2020.00052
S Alex Marshall 1 , Justin A McClain 1 , Jessica I Wooden 2 , Kimberly Nixon 1, 2
Affiliation  

Microglia are dynamic cells that have roles in neuronal plasticity as well as in recovery responses following neuronal injury. Although many hypothesize that hyperactivation of microglia contributes to alcohol-induced neuropathology, in other neurodegenerative conditions disruption of normal microglial processes also contributes to neuronal loss, particularly as microglia become dystrophic or dysfunctional. Based on the observation of a striking, abnormal morphology in microglia during binge-like ethanol exposure, the present study investigated the impact of excessive ethanol exposure on microglia number and dystrophic morphology in a model of alcohol dependence that includes neurodegeneration in both adult and adolescent rats. Following 2- and 4-day binge ethanol exposure, the number of microglia was decreased in the hippocampus and the perirhinal and entorhinal cortices of both adult and adolescent rats. Furthermore, a significant number of microglia with a dystrophic morphology were observed in ethanol-exposed tissue, accompanied by a significant decrease in brain-derived neurotrophic factor (BDNF) expression in the hippocampus. Together these findings suggest another means by which microglia may contribute to alcohol-induced neurodegeneration, specifically dystrophic microglia and/or loss of microglia may disrupt homeostatic and recovery mechanisms. These results demonstrate that microglia also degenerate with excessive alcohol exposure, which has important implications for understanding the role of microglia-and specifically their contributions to plasticity and neuronal survival-in neurodegenerative disease.

中文翻译:

青少年和成年雄性大鼠酗酒后的小胶质细胞营养不良。

小胶质细胞是动态细胞,在神经元可塑性以及神经元损伤后的恢复反应中发挥作用。尽管许多人假设小胶质细胞的过度活化会导致酒精引起的神经病理学,但在其他神经退行性疾病中,正常小胶质细胞过程的破坏也会导致神经元丢失,特别是当小胶质细胞变得营养不良或功能失调时。基于在暴饮暴食乙醇暴露期间观察到的小胶质细胞显着异常形态,本研究调查了过量乙醇暴露对酒精依赖模型中小胶质细胞数量和营养不良形态的影响,该模型包括成年和青春期大鼠的神经变性. 在 2 天和 4 天的酒精暴饮暴食之后,成年和青春期大鼠的海马体以及周围和内嗅皮质中的小胶质细胞数量减少。此外,在暴露于乙醇的组织中观察到大量具有营养不良形态的小胶质细胞,伴随着海马中脑源性神经营养因子 (BDNF) 表达的显着降低。这些发现共同表明小胶质细胞可能有助于酒精诱导的神经变性的另一种方式,特别是营养不良的小胶质细胞和/或小胶质细胞的丧失可能会破坏体内平衡​​和恢复机制。这些结果表明,小胶质细胞也会随着过度饮酒而退化,这对于理解小胶质细胞的作用——尤其是它们对神经退行性疾病中可塑性和神经元存活的贡献——具有重要意义。
更新日期:2020-08-13
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