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Neuroprotective effect of high glucose against NMDA, free radical, and oxygen-glucose deprivation through enhanced mitochondrial potentials.

Authors
Seo, SY; Kim, EY; Kim, H; Gwag, BJ
Citation
The Journal of neuroscience : the official journal of the Society for Neuroscience, 19(20):8849-8855, 1999
Journal Title
The Journal of neuroscience : the official journal of the Society for Neuroscience
ISSN
0270-64741529-2401
Abstract
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 [Ca(2+)](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.
MeSH terms
AnimalsAnoxia/pathologyAnoxia/physiopathology*Cells, CulturedCerebral Cortex/drug effectsCerebral Cortex/pathologyElectrophysiologyExcitatory Amino Acid Agonists/pharmacology*Glucose/administration & dosage*Glucose/deficiency*Glucose/pharmacologyMiceMice, Inbred ICRMitochondria/physiology*N-Methylaspartate/pharmacology*Neurons/drug effectsNeurons/physiologyNeuroprotective Agents/pharmacology*Neurotoxins/metabolismNeurotoxins/pharmacology*Reactive Oxygen Species/metabolism*
PMID
10516304
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
AJOU Authors
곽, 병주
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