Mitochondrial transmembrane potential and free radical production in excitotoxic neurodegeneration

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Abstract
Excitotoxic cell death is involved in many forms of acute and chronic neurodegeneration. We induced excitotoxic cell death in cultured rat hippocampal neurons by brief exposure to two selective glutamate receptor agonists with different neurotoxic potencies, N-methyl-d-aspartate (NMDA) and kainate (KA). Digital video imaging was performed during exposure to the agonists to monitor free radical production and changes in mitochondrial transmembrane potential, Ψm. Brief exposure to NMDA (10min) induced significant cell death in the hippocampal neurons reaching a maximum at a concentration of 300μM (57.2±2.6% cell death; PPm in 70.1±10.1% of the hippocampal neurons during the exposure to NMDA. In contrast to NMDA, brief exposure to KA (10min) produced limited neurotoxicity reaching a maximum at a concentration of 100μM (10.2±4.0% cell death; PPm in only 13.5±1.4% of the hippocampal neurons. In conclusion, the present study demonstrates that early changes in intracellular superoxide production and Ψm relate to neuronal survival outcome in excitotoxic cell death.

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