Ischemic Tolerance in Murine Cortical Cell Culture: Critical Role for NMDA Receptors

Murine cortical cultures containing both neurons and glia (days in vitro 13-15) were exposed to periods of oxygen-glucose deprivation (5-30 min) too brief to induce neuronal death. Cultures "preconditioned" by sublethal oxygen-glucose deprivation exhibited 30-50% less neuronal death than c...

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Bibliographic Details
Published in:The Journal of neuroscience 1999-03, Vol.19 (5), p.1657-1662
Main Authors: Grabb, Margaret C, Choi, Dennis W
Format: Article
Language:English
Subjects:
Animals
Brain Ischemia - metabolism
Cell Death - drug effects
Cell Hypoxia - physiology
Cells, Cultured
Cerebral Cortex - cytology
Cerebral Cortex - drug effects
Cerebral Cortex - metabolism
Dizocilpine Maleate - pharmacology
Excitatory Amino Acid Agonists - pharmacology
Excitatory Amino Acid Antagonists - pharmacology
Fetus
Glucose - metabolism
Mice
N-Methylaspartate - antagonists & inhibitors
N-Methylaspartate - pharmacology
Neurons - cytology
Neurons - drug effects
Neurons - metabolism
Neuroprotective Agents - pharmacology
Piperazines
Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors
Receptors, N-Methyl-D-Aspartate - metabolism
Receptors, N-Methyl-D-Aspartate - physiology
Time Factors
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Summary:Murine cortical cultures containing both neurons and glia (days in vitro 13-15) were exposed to periods of oxygen-glucose deprivation (5-30 min) too brief to induce neuronal death. Cultures "preconditioned" by sublethal oxygen-glucose deprivation exhibited 30-50% less neuronal death than controls when exposed to a 45-55 min period of oxygen-glucose deprivation 24 hr later. This preconditioning-induced neuroprotection was specific in that neuronal death induced by exposure to excitotoxins or to staurosporine was not attenuated. Neuroprotection was lost if the time between the preconditioning and severe insult were decreased to 7 hr or increased to 72 hr and was blocked if the NMDA antagonist 100 microM 3-((D)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid was applied during the preconditioning insult. This was true even if the duration of preconditioning was increased as far as possible (while still remaining sublethal). A similar preconditioning effect was also produced by sublethal exposure to high K+, glutamate, or NMDA but not to kainate or trans-1-aminocyclopentane-1, 3-dicarboxylic acid.
ISSN:0270-6474
1529-2401
DOI:10.1523/jneurosci.19-05-01657.1999