作者: Samantha L. Budd
DOI: 10.1016/S0163-7258(98)00029-1
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摘要: Following a hypoxic-ischemic insult, the collapse of ion gradients results in inappropriate release excitatory neurotransmitters. Although amino acids such as glutamate are likely extracellular mediators ensuing neuronal cell death, intracellular events occurring downstream receptor activation much less clear. The present review attempts to summarize how Ca2+ overload neurons following insult is neurotoxic. In particular, interlocked relation between mitochondrial accumulation and subsequent death examined.