Neuronal death after ischemia-induced brain damage depends largely upon the activation
of the N-methyl-D-aspartate (NMDA) excitatory glutamate receptor that is a target for many …

Despite the beneficial effects of prototypical glutamatergic receptor antagonists in animal
models, the pharmacological attempts by the use of such agents have met with very limited …

Measurements and Main Results: Here, we show using multiple models of ex vivo and in
vivo excitotoxic insults and brain ischemia that nitrous oxide, administered alone at …

Excess activation of ionotropic glutamate receptors, primarily N-methyl-D-aspartate (NMDA)
receptors and free radicals, evoke nerve cell death following hypoxic-ischemic brain injury in …

Recent evidence in primary neuronal cell culture implicates nitric oxide (NO) as a mediator
of glutamatergic neurotoxicity acting via N-methyl-D-aspartate (NMDA) receptors. We find …

Tissue responses to ischemia influx into neurons. The gating of glutamate receptor–
activated channels effectively achieves membrane shunting, which spreads in waves …

An accumulation of experimental data suggests that N-methyl-D-aspartate (NMDA) receptor
antagonists will prevent ischemic neuronal injury following transient global ischemia and …

Excitotoxicity and oxidative stress mediate neuronal death after hypoxic—ischemic brain
injury. We examined the possibility that targeting both N-methyl-d-aspartate (NMDA) …

Sublethal ischemic challenges can protect neurons against a second, more severe hypoxic
insult. We report here that nonlethal chemical ischemia induces a transient alteration of …

Ischemic brain injury produced by stroke or cardiac arrest is a major cause of human
neurological disability. Steady advances in the neurosciences have elucidated …