Abstract
Neuron-enriched cultures from embryonic rat cerebral cortex were exposed to hypoxia and hypoglycemia, and the resulting cellular injury was quantified by measuring lactate dehydrogenase (LDH) release, which was maximal after 20-24 h. The increase in LDH release produced by hypoxia/hypoglycemia was prevented by N-methyl-D-aspartate (NMDA) antagonists, but not by three classes of drugs thought to modulate glutamate release: Ca2+ channel antagonists (nimodipine, omega-conotoxin GVIA, omega-agatoxin-IVA), KATP channel activators (cromakalim, diazoxide), and glutamate transport inhibitors (dihydrokainate, DL-threo-beta-hydroxyaspartate).
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Aspartic Acid / analogs & derivatives
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Aspartic Acid / pharmacology
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Benzopyrans / pharmacology
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Calcium Channel Blockers / pharmacology
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Cell Hypoxia
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Cells, Cultured
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Cerebral Cortex / physiology*
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Cromakalim
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Diazoxide / pharmacology
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Embryo, Mammalian
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Glutamates / metabolism
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Hypoglycemia
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Kainic Acid / analogs & derivatives
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Kainic Acid / pharmacology
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Kinetics
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L-Lactate Dehydrogenase / analysis
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Neurons / drug effects
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Neurons / physiology*
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Potassium Channels / drug effects
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Potassium Channels / physiology
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Pyrroles / pharmacology
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Quinoxalines / pharmacology
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Rats
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Rats, Sprague-Dawley
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Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors
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Synapses / drug effects
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Synapses / physiology*
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Synaptic Transmission / drug effects
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Synaptic Transmission / physiology*
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Time Factors
Substances
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Benzopyrans
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Calcium Channel Blockers
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Glutamates
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Potassium Channels
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Pyrroles
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Quinoxalines
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Receptors, N-Methyl-D-Aspartate
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Cromakalim
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3-hydroxyaspartic acid
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Aspartic Acid
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dihydrokainic acid
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FG 9041
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L-Lactate Dehydrogenase
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Diazoxide
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Kainic Acid