期刊
NEUROSCIENTIST
卷 10, 期 1, 页码 18-25出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/1073858403255840
关键词
nitric oxide; oxidative stress; cerebral ischemia; metal chelator; zinc
资金
- NINDS NIH HHS [NS40215, NS38585, NS042882, NS41682] Funding Source: Medline
It has been nearly 15 years since the suggestion that synaptically released Zn2+ might contribute to excitotoxic brain injury after seizures, stroke, and brain trauma. In the original zinc-translocation model, it was proposed that synaptically released Zn2+ ions penetrated postsynaptic neurons, causing injury. According to the model, chelating zinc in the cleft was predicted to be neuroprotective. This proved to be true: zinc chelators have proved to be remarkably potent at reducing excitotoxic neuronal injury in many paradigms. Promising new zinc-based therapies for stroke, head trauma, and epileptic brain injury are under development. However, new evidence suggests that the original translocation model was incomplete. As many as three sources of toxic zinc ions may contribute to excitotoxicity: presynaptic vesicles, postsynaptic zinc-sequestering proteins, and (more speculatively) mitochondrial pools. The authors present a new model of zinc currents and zinc toxicity that offers expanded opportunities for zinc-selective therapeutic chelation interventions.
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