Neuronal apoptosis after CNS injury: The roles of glutamate and calcium

被引：223

作者：

Zipfel, GJ

Babcock, DJ

Lee, JM

Choi, DW

机构：

[1] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA

[2] Washington Univ, Sch Med, Ctr Study Nervous Syst Injury, St Louis, MO 63110 USA

来源：

JOURNAL OF NEUROTRAUMA | 2000年 / 17卷 / 10期

关键词：

trauma; ischemia; stroke; hypoxia; apoptosis; excitotoxicity; neuroprotection;

D O I：

10.1089/neu.2000.17.857

中图分类号：

R4 [临床医学];

学科分类号：

1002 ; 100602 ;

摘要：

While a role has been well established for excitotoxic necrosis in the pathogenesis of traumatic or ischemic damage to the CNS, accumulating evidence now suggests that apoptosis may also be a prominent contributor. In this review we focus on the role of glutamate and attendant intracellular calcium influx in triggering or modifying excitotoxic necrosis and apoptosis, raising the possibility that calcium influx may affect these two death pathways in opposite directions. Incorporating consideration of both pathways will probably be needed to develop the most effective neuroprotective treatments for CNS injury.

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收藏

页码：857 / 869

页数：13

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