小胶质细胞
神经退行性变
神经突
星形胶质细胞
神经科学
神经胶质
生物
海马结构
氧化应激
神经元
中枢神经系统
医学
内分泌学
病理
炎症
免疫学
体外
生物化学
疾病
作者
Larry C.H. Park,Hui Zhang,Gary E. Gibson
标识
DOI:10.1016/s0047-6374(01)00336-0
摘要
Thiamine deficiency (TD) is a model of chronic impairment of oxidative metabolism that leads to neurodegeneration. TD induces oxidative stress and death in neurons, but does not kill astrocytes, microglia or brain endothelial cells. TD primary hippocampal neurons were either cultured alone, or co-cultured with primary astrocytes or microglia. After 7 days of TD, 50% of the neurons died, and the processes of many of the surviving neurons were severely truncated. When TD neurons were co-cultured with astrocytes or microglia, neurons did not die nor show decreased neurite outgrowth. Thus, neuronal-glial interactions are critical for maintaining neuronal homeostasis during chronic metabolic impairment.
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