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Zn(2+)-induced disruption of neuronal mitochondrial function: synergism with Ca(2+), critical dependence upon cytosolic Zn(2+) buffering, and contributions to neuronal injury
Excitotoxic Zn(2+) and Ca(2+) accumulation contributes to neuronal injury after ischemia or prolonged seizures. Synaptically released Zn(2+) can enter postsynaptic neurons via routes including voltage sensitive Ca(2+) channels (VSCC), and, more rapidly, through Ca(2+) permeable AMPA channels. There...
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| Pubblicato in: | Exp Neurol |
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| Autori principali: | , |
| Natura: | Artigo |
| Lingua: | Inglês |
| Pubblicazione: |
2018
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| Soggetti: | |
| Accesso online: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5849513/ https://ncbi.nlm.nih.gov/pubmed/29355498 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.expneurol.2018.01.012 |
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