Neurodegeneration mediated by glutamate and beta-amyloid peptide: a comparison and possible interaction
Abstract
In Alzheimer's disease, abnormal extracellular accumulations of beta-amyloid (a major component of the senile plaques) and of the excitatory amino acid glutamate are both thought to be associated with degeneration of nerve cells. In the present study, using cultured cortical or hippocampal neurons as an in vitro model, we compared the effects of various factors influencing neurodegeneration mediated by glutamate or by beta-amyloid peptide (A beta). We also asked the question: does long-term treatment with sublethal doses of A beta-(25-35) potentiate glutamate-mediated excitotoxicity? Neuronal cell death was quantified using the lactate dehydrogenase (LDH) method. Since extracellular LDH remains stable for days, the magnitude of relative afflux of LDH correlates in a linear fashion with the number of damaged neurons in cultures. When applied singly, both glutamate (for 15 min) and A beta-(25-35) or its parent peptide A beta-(1-40) (continuously) produced a dose-dependent neuronal degeneration. In the case of glutamate, the half-maximal effects were observed at about 0.08 mM glutamate for both cerebral cortical and hippocampal neurons (cultured for 13 days in vitro, DIV). The effect of A beta-(25-35) was also time-dependent, whil...Continue Reading
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