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NMDA receptors are a key component in mediating glutamate-induced [excitotoxicity]], and it is believed that NMDA antagonists would be neuroprotective after a stroke or other traumatic brain injury. After a traumatic brain injury, neurons become deprived of glucose and oxygen. These neurons quickly lose ATP and become depolarized, which releases glutamate. The intracellular buildup of glutamate trigger the overstimulation of AMPA and NMDA receptors. This, in turn, causes an influx of Na+ and Ca+. Therefore, when NMDA receptors are activated, there is an increase in intracellular Ca+ concentration. High Ca+ causes fatal metabolic consequences, including neuronal cell death.
- The Pharma Letter. 2 December 1996 Synthelabo's Eliprodil Fails In Stroke Trials
- DeKeyser J, Sulter G, & Luiten PG (1999) Clinical trials with neuroprotective drugs in acute ischaemic stroke: are we doing the right thing? Trends in neurosciences 22(12):535-540 PMID 10542428
- Lee JM, Zipfel GJ, & Choi DW (1999) The changing landscape of ischaemic brain injury mechanisms. Nature 399(6738 Suppl):A7-14 PMID 10392575
- Ikonomidou C & Turski L (2002) Why did NMDA receptor antagonists fail clinical trials for stroke and traumatic brain injury? The Lancet. Neurology 1(6):383-386 PMID 12849400
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