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.
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.
NMDA receptor antagonists are a class of anesthetics that work to antagonize, or inhibit the action of, the N-methyl d-aspartate receptor (NMDAR). They are used as anesthesia for animals and, less commonly, for humans; the state of anesthesia they induce is referred to as dissociative anesthesia. Memantine is an uncompetitive NMDA channel blocker. Memantine is the first in a novel class of Alzheimer's disease medications acting on the glutamatergic system by blocking NMDA glutamate…
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.
ScienceDirect.com - Vision Research - Neurochemical organization of the macaque retina: effect of TTX on levels and gene expression of cytochrome oxidase and nitric oxide synthase and on the immunoreactivity of Na+K+ATPase and NMDA receptor subunit I