nice Cryo-EM structures of the triheteromeric NMDA receptor and its allosteric modulation Check more at https://epeak.info/2017/03/23/cryo-em-structures-of-the-triheteromeric-nmda-receptor-and-its-allosteric-modulation/
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.
A translational approach for NMDA receptor profiling as a vulnerability biomarker for depression and schizophrenia - Gunduz-Bruce - 2017 - Experimental Physiology - Wiley Online Library
Gathering the clues to rare gene variants contributing to schizophrenia February 21st Schizophrenia has long been known to be highly heritable and is present in approximately 1% of the population. Researchers have been following two paths in their pursuit of identifying schizophrenia risk genes. - See more at: http://allblackclothes.com/index.php?cID=159#sthash.YJBzfCQA.dpuf
A new pharmaceutical technology licensed in February by the Corporate Ventures office at The Hospital for Sick Children (SickKids) may help treat neuropathic and inflammatory pain in children and adults, but without the serious side effects that can accompany currently available treatments.
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.