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Excitotoxic insult results in a long-lasting activation of CaMKIIα and mitochondrial damage in living hippocampal neurons.
Over-activation of excitatory NMDA receptors and the resulting Ca2+ overload is the main cause of neuronal toxicity during stroke. CaMKII becomes misregulated during such events. Biochemical studies show either a dramatic loss of CaMKII activity or its persistent autonomous activation after stroke,...
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主要な著者: | , , , , , |
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フォーマット: | Artigo |
言語: | Inglês |
出版事項: |
Public Library of Science (PLoS)
2015-01-01
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シリーズ: | PLoS ONE |
オンライン・アクセス: | http://europepmc.org/articles/PMC4368532?pdf=render |
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