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- W2766365536 abstract "Our previous study demonstrated that colchicine-induced dentate granule cell death is caused by blocking axonal flow and the accumulation of intracellular zinc. Zinc is concentrated in the synaptic vesicles via zinc transporter 3 (ZnT3), which facilitates zinc transport from the cytosol into the synaptic vesicles. The aim of the present study was to identify the role of ZnT3 gene deletion on colchicine-induced dentate granule cell death. The present study used young (3–5 months) mice of the wild-type (WT) or the ZnT3−/− genotype. Colchicine (10 µg/kg) was injected into the hippocampus, and then brain sections were evaluated 12 or 24 h later. Cell death was evaluated by Fluoro-Jade B; oxidative stress was analyzed by 4-hydroxy-2-nonenal; and dendritic damage was detected by microtubule-associated protein 2. Zinc accumulation was detected by N-(6-methoxy-8-quinolyl)-para-toluenesulfonamide (TSQ) staining. Here, we found that ZnT3−/− reduced the number of degenerating cells after colchicine injection. The ZnT3−/−-mediated inhibition of cell death was accompanied by suppression of oxidative injury, dendritic damage and zinc accumulation. In addition, ZnT3−/− mice showed more glutathione content than WT mice and inhibited neuronal glutathione depletion by colchicine. These findings suggest that increased neuronal glutathione by ZnT3 gene deletion prevents colchicine-induced dentate granule cell death." @default.
- W2766365536 created "2017-11-10" @default.
- W2766365536 creator A5045108032 @default.
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- W2766365536 date "2017-10-19" @default.
- W2766365536 modified "2023-10-16" @default.
- W2766365536 title "ZnT3 Gene Deletion Reduces Colchicine-Induced Dentate Granule Cell Degeneration" @default.
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- W2766365536 doi "https://doi.org/10.3390/ijms18102189" @default.
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