Pre-and post-synaptic modulators of excitatory neurotransmission: comparative effects on hypoxia/hypoglycemia in cortical cultures
B Koretz, KB Ahern, N Wang, HS Lustig, DA Greenberg - Brain research, 1994 - Elsevier
B Koretz, KB Ahern, N Wang, HS Lustig, DA Greenberg
Brain research, 1994•ElsevierNeuron-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: Ca 2+ channel antagonists (nimodipine, ω-conotoxin GVIA, ω-agatoxin-IVA), K ATP …
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: Ca 2+ channel antagonists (nimodipine, ω-conotoxin GVIA, ω-agatoxin-IVA), K ATP …
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, ω-conotoxin GVIA, ω-agatoxin-IVA), KATP channel activators (cromakalim, diazoxide), and glutamate transport inhibitors (dihydrokainate, dl-threo-β-hydroxyaspartate).
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