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- W1569014924 endingPage "837" @default.
- W1569014924 startingPage "821" @default.
- W1569014924 abstract "Increased levels of intracellular zinc have been implicated in neuronal cell death in ischaemia, epilepsy and traumatic brain damage. However, decreases in zinc levels also lead to increased neuronal death and lowered seizure threshold. In the present study we investigated the physiological role of zinc in neurodegeneration and protection following epileptic seizures. Cells located in the strata oriens and lucidum of the CA3 region accumulated high concentrations of zinc and died. A decrease in zinc level could prevent the death of these neurones after seizures. Most of these cells were GABAergic interneurones. In contrast, neurones in the CA3 pyramidal cell layer accumulated moderate amounts of zinc and survived. Zinc chelation led to an increase in the mortality rate of these cells. Furthermore, in these cells low concentrations of intracellular zinc activated Akt (protein kinase B), thus providing protection against neurodegeneration. These results demonstrate that intracellularly accumulated zinc can be neurotoxic or neuroprotective depending on its concentration. This dual action is cell type specific." @default.
- W1569014924 created "2016-06-24" @default.
- W1569014924 creator A5045660580 @default.
- W1569014924 creator A5053771439 @default.
- W1569014924 creator A5054942236 @default.
- W1569014924 creator A5067401002 @default.
- W1569014924 creator A5076972889 @default.
- W1569014924 creator A5083717705 @default.
- W1569014924 date "2005-07-27" @default.
- W1569014924 modified "2023-10-15" @default.
- W1569014924 title "Cell type-specific action of seizure-induced intracellular zinc accumulation in the rat hippocampus" @default.
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