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长期应用铝诱导大鼠大脑皮质培养神经元的功能和形态学变化。

Functional and morphological changes in cultured neurons of rat cerebral cortex induced by long-term application of aluminum.

作者信息

Kawahara M, Muramoto K, Kobayashi K, Kuroda Y

机构信息

Department of Molecular and Cellular Neurobiology, Tokyo Metropolitan Institute for Neuroscience, Japan.

出版信息

Biochem Biophys Res Commun. 1992 Dec 30;189(3):1317-22. doi: 10.1016/0006-291x(92)90217-9.

Abstract

Aluminum is an environmental neurotoxin and a suspected risk factor for Alzheimer's disease. The neurotoxicity of aluminum on cultured neurons of rat cerebral cortex was investigated using an assay system for synapse formation and immunohistochemistry. The frequency of spontaneous oscillations of intracellular Ca2+, which is correlated to the number of synapses, was decreased after exposure to 100 microM of aluminum chloride for 22 days. Long-term application of aluminum (48 days) caused aggregation of cell bodies and fasciculation of processes. Processes and cell bodies were strongly stained by antibody to tau protein, which is one of the main components of Alzheimer's neurofibrillary tangles. It is suggested that the characteristics of the degeneration of cultured neurons induced by aluminum show some similarities to the pathology observed in brains with Alzheimer's disease.

摘要

铝是一种环境神经毒素,也是阿尔茨海默病的可疑风险因素。利用突触形成检测系统和免疫组织化学方法,研究了铝对大鼠大脑皮层培养神经元的神经毒性。与突触数量相关的细胞内Ca2+自发振荡频率,在暴露于100微摩尔氯化铝22天后降低。长期应用铝(48天)导致细胞体聚集和突起成束。突起和细胞体被tau蛋白抗体强烈染色,tau蛋白是阿尔茨海默病神经原纤维缠结的主要成分之一。提示铝诱导的培养神经元退化特征与阿尔茨海默病大脑中观察到的病理学有一些相似之处。

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