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BCL-2 blocks glutamate toxicity in neural cell lines
L T Zhong1, D J Kane, D E Bredesen
1Department of Neurology, UCLA School of Medicine 90024-1769.
Brain Research. Molecular Brain Research
|September 1, 1993
Summary
High glutamate concentrations kill central neural cell lines. Expressing the bcl-2 gene protected these cells from glutamate neurotoxicity, suggesting a role for bcl-2 in neuronal survival.
Area of Science:
- Neuroscience
- Cell Biology
- Molecular Biology
Background:
- Glutamate is a key neurotransmitter.
- High concentrations of glutamate can cause excitotoxicity and neuronal death.
- The pheochromocytoma cell line PC12 is a common model for neuronal studies.
Purpose of the Study:
- To investigate the effect of high glutamate concentrations on immortalized central neural cell lines.
- To determine if the proto-oncogene bcl-2 can protect neural cells from glutamate neurotoxicity.
- To examine the protective effect of potassium chloride on glutamate toxicity in different neuronal cell lines.
Main Methods:
- Utilized immortalized central neural cell lines and the PC12 cell line.
- Exposed cells to high concentrations of glutamate (5-10 mM).
- Investigated the role of bcl-2 expression in cellular resistance to glutamate.
- Tested the neuroprotective effects of potassium chloride (25 mM).
Main Results:
- High glutamate concentrations induced cell death in immortalized central neural cell lines, similar to PC12 cells.
- The expression of the proto-oncogene bcl-2 significantly blocked glutamate-induced neurotoxicity.
- Potassium chloride (25 mM) protected a cerebellar neuronal cell line but not PC12 cells from glutamate toxicity.
Conclusions:
- Glutamate neurotoxicity affects various immortalized central neural cell lines.
- The proto-oncogene bcl-2 plays a protective role against glutamate excitotoxicity.
- Differential effects of potassium chloride suggest cell-type specific mechanisms in glutamate toxicity response.