B. Koretz et al., PRESYNAPTIC AND POSTSYNAPTIC MODULATORS OF EXCITATORY NEUROTRANSMISSION - COMPARATIVE EFFECTS ON HYPOXIA HYPOGLYCEMIA IN CORTICAL CULTURES/, Brain research, 643(1-2), 1994, pp. 334-337
Neuron-enriched cultures from embryonic rat cerebral cortex were expos
ed 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 hypoxi
a/hypoglycemia was prevented by N-methyl-D-aspartate (NMDA) antagonist
s, but not by three classes of drugs thought to modulate glutamate rel
ease: Ca2+ channel antagonists (nimodipine, omega-conotoxin GVIA, omeg
a-agatoxin-IVA), K-ATP channel activators (cromakalim, diazoxide), and
glutamate transport inhibitors (dihydrokainate, DL-threo-beta-hydroxy
aspartate).