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The Journal of Neuroscience, October 15, 1999, 19(20):8849-8855

Neuroprotective Effect of High Glucose Against NMDA, Free Radical, and Oxygen-Glucose Deprivation through Enhanced Mitochondrial Potentials

So Y. Seo¹, Eun Y. Kim¹, Harriet Kim², and Byoung J. Gwag¹

¹ Department of Pharmacology, Ajou University School of Medicine, Suwon, Kyungkido, 442-749 Korea, and ² Department of Food and Nutrition, College of Human Ecology, Seoul National University, Seoul, 151-742 Korea

Cultured cortical neurons maintained in 25 mM glucose underwent a widespread neuronal death after exposure to NMDA, AMPA, and kainate. Among these, NMDA toxicity was substantially reduced in neurons maintained in 100 mM glucose. NMDA-induced increase in [Ca²⁺]_i and reactive oxygen species was attenuated in neurons maintained in high glucose that revealed increased mitochondrial membrane and redox potentials as determined using rhodamine 123 and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide. p-trifluoromethoxy-phenylhydrazone, KCN, and rotenone, the selective inhibitors of mitochondrial potential, abrogated neuroprotective effect of high glucose against NMDA. The neuroprotective action of high glucose was extended against oxygen or combined oxygen-glucose deprivation. The present study provides evidence that prolonged exposure of cortical cells to high glucose attenuates NMDA- and free radical-mediated neuronal death via enhanced mitochondrial function.

Key words: glucose; mitochondria; membrane potential; redox potential; excitotoxicity; Ca²⁺; reactive oxygen species; ischemia

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Copyright © 1999 Society for Neuroscience  0270-6474/99/19208849-07$05.00/0

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