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The role of zinc in selective neuronal death after transient global cerebral ischemia.

Authors
Koh, JY; Suh, SW; Gwag, BJ; He, YY; Hsu, CY; Choi, DW
Citation
Science, 272(5264):1013-1016, 1996
Journal Title
Science
ISSN
0193-4511
Abstract
Zinc is present in presynaptic nerve terminals throughout the mammalian central nervous system and likely serves as an endogenous signaling substance. However, excessive exposure to extracellular zinc can damage central neurons. After transient forebrain ischemia in rats, chelatable zinc accumulated specifically in degenerating neurons in the hippocampal hilus and CA1, as well as in the cerebral cortex, thalamus, striatum, and amygdala. This accumulation preceded neurodegeneration, which could be prevented by the intraventricular injection of a zinc chelating agent. The toxic influx of zinc may be a key mechanism underlying selective neuronal death after transient global ischemic insults.
MeSH terms
AminoquinolinesAnimalsBrain/metabolism/*pathologyCell DeathChelating Agents/pharmacologyDithizone/pharmacologyEdetic Acid/pharmacologyFluorescent DyesHippocampus/metabolism/pathologyIschemic Attack, Transient/*metabolism/*pathologyMicroscopy, Fluorescence*Nerve DegenerationNeurons/metabolism/*pathologyPresynaptic Terminals/metabolismPyramidal Cells/metabolism/pathologyRatsTosyl CompoundsZinc/*metabolism
PMID
8638123
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
AJOU Authors
곽, 병주
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