Park L C, Zhang H, Gibson G E
Department of Neurology and Neuroscience, Weill Medical College of Cornell University at Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA.
Mech Ageing Dev. 2001 Dec;123(1):21-7. doi: 10.1016/s0047-6374(01)00336-0.
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.
硫胺素缺乏症（TD）是一种慢性氧化代谢受损导致神经退行性变的模型。TD会诱导神经元发生氧化应激和死亡，但不会杀死星形胶质细胞、小胶质细胞或脑内皮细胞。TD原代海马神经元要么单独培养，要么与原代星形胶质细胞或小胶质细胞共培养。TD处理7天后，50%的神经元死亡，许多存活神经元的突起严重缩短。当TD神经元与星形胶质细胞或小胶质细胞共培养时，神经元不会死亡，神经突生长也不会减少。因此，在慢性代谢受损期间，神经胶质细胞间的相互作用对于维持神经元内环境稳定至关重要。
