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剩余呼吸能力、氧化应激和兴奋毒性。

Spare respiratory capacity, oxidative stress and excitotoxicity.

机构信息

Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA.

出版信息

Biochem Soc Trans. 2009 Dec;37(Pt 6):1385-8. doi: 10.1042/BST0371385.

DOI:10.1042/BST0371385
PMID:19909281
Abstract

Chronic exposure to glutamate (glutamate excitotoxicity) exacerbates neuronal damage in the aftermath of stroke and is implicated in a variety of neurodegenerative disorders. Mitochondria play a central role in the survival or death of the exposed neuron. Calcium, oxidative stress and ATP insufficiency play closely interlocked roles that may be investigated with primary neuronal cultures.

摘要

慢性暴露于谷氨酸(谷氨酸兴奋性毒性)会加剧中风后的神经元损伤,并与多种神经退行性疾病有关。线粒体在暴露神经元的存活或死亡中起着核心作用。钙、氧化应激和 ATP 不足起着紧密相关的作用,可以通过原代神经元培养来研究这些作用。

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