Mechanisms of neuronal damage in brain hypoxia/ischemia: focus on the role of mitochondrial calcium accumulation.
Following a hypoxic-ischemic insult, the collapse of ion gradients results in the inappropriate release of excitatory neurotransmitters. Although excitatory amino acids such as glutamate are the likely extracellular mediators of the ensuing neuronal cell death, the intracellular events occurring downstream of glutamate receptor activation are much less clear. The present review attempts to summarize how Ca2+ overload of neurons following a hypoxic-ischemic insult is neurotoxic. In particular, the interlocked relation between mitochondrial Ca2+ accumulation and subsequent neuronal cell death is examined.
Budd
S L
SL
Neurosciences Institute, Ninewells Medical School, University of Dundee, Scotland, UK.
D000818:Animals; D017209:Apoptosis; D002545:Brain Ischemia / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism*; D018698:Glutamic Acid / Q000633:toxicity; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D008959:Models, Neurological; D009474:Neurons / Q000378:metabolism*
D018698:Glutamic Acid; D002118:Calcium