Molecular engineering can generate light-sensitive NMDA receptors with specific subunit combinations.

Ketamine, an NMDA receptor antagonist and experimental model for schizophrenia, produces decision-making deficits in monkeys, which are predicted by a lowering of cortical excitation-inhibition balance in a spiking circuit model.

The small molecule NMDA-receptor antagonist MK801 has been genetically targeted to specific cell types in brain tissue to examine the role of NMDA receptors in cocaine-induced synaptic plasticity.

NMDARs promote spine formation to control survival of adult-born granule cells, but gauge spine enlargement and recruitment of AMPARs in both developing and mature neurons.

The rapid antidepressant actions of low dose ketamine occur through the direct relief of suppression of protein synthesis via antagonism of a subset of NMDA receptors containing the GluN2B subunit.

Molecular dynamics simulations reveal that D-serine competes with glutamate for binding to the NMDA receptor, a finding supported by electrophysiology experiments with consequences for D-serine-focused therapeutic strategies for myriad neurological disorders.

LAR-RPTPs are not essential for synapse formation, but they are important determinants of synapse properties as they contribute to regulate postsynaptic NMDA receptor function.

Presynaptic adhesion molecule PTPσ in the hippocampus regulates postsynaptic NMDA receptor function and behavioral novelty recognition through mechanisms independent of their trans-synaptic binding partners.

D-serine has a major role in the regulation of NMDA receptors not only contributing to its activation as the receptors co-agonist, but also by regulating specifically GluN2B-NMDA receptor trafficking and synaptic content at developing hippocampal synapses.

Excitotoxicity driven by NMDA receptor hyper-activation does not involve DAPK1-dependent events in vitro or in vivo, and previously described DAPK1-NMDAR disrupting peptides act by blocking the NMDA receptor.