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NMDA (N-methyl-D-aspartate) is the selective agonist that binds to NMDA receptors but not to other glutamate receptors. The NMDA receptor (NMDAR) is the predominant molecular device for controlling synaptic plasticity and memory function. The NMDAR is a type of ionotropic glutamate receptor. Activation of NMDA receptors requires binding of glutamate or aspartate (aspartate does not stimulate the receptors as strongly). In addition, NMDARs also require the binding of the co-agonist glycine.


Blocking NMDA receptors to limit neurotoxicity January 24th Structural biologists at Cold Spring Harbor Laboratory (CSHL) and collaborators at Emory University have obtained important scientific results likely to advance efforts to develop new drugs targeting NMDA receptors in the brain. - See more at:

Wind-up pain is caused by activation of normally dormant NMDA receptors.Activated NMDA receptors cause - influx of Calcium into Dorsal Horn Wide Dynamic Range interneurons resulting in a cycle of - increased production/sensitization/number of NMDA receptors & increased release of Glutamate/Substance-P at presynaptic sites This positive feedback loop results in a marked increase in the pain signal ultimately perceived by the brain.

My friend, Duncan Momaney coauthored this published paper at age 22!!! I bow humbly before a man who works hard to advance knowledge! - The uncompetitive NMDA receptor antagonists ketamine and memantine preferentially increase the choice for a small, immediate reward in low-impulsive rats


Dallas Cowboy Amobi Okoye recovers from NMDA receptor encephalitis Posted August 24, 2014 by Will McDow in News


New drug reverses loss of brain connections in Alzheimer's

Aβ induces astrocytic glutamate release, extrasynaptic NMDA receptor activation, and synaptic loss

Antagonism of NMDA receptors as a potential treatment for Down syndrome: a pilot randomized controlled trial & links to similar articles

There is evidence that NMDA receptor antagonists can cause a certain type of neurotoxicity or brain damage referred to as Olney's Lesions in rodents, although such damage has never been conclusively observed in primates like humans. However, adolescent cynomolgus monkeys that were injected daily for six months with the non-competitive NMDA antagonist ketamine showed decreased locomotor activity and increased apoptosis of cells in their prefrontal cortices.