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.

NMDA receptor function is regulated by protein depalmitoylation during visual cortical maturation and is dysfunctional in infantile neuronal ceroid lipofuscinosis.

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

Novel spatial representations by hippocampal cellular assemblies develop on the framework of preconfigured hippocampal networks whose homeostatic synaptic reorganization is accelerated by prior experience and CA3 NMDAR-dependent plasticity.

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.

An activity-dependent mechanism sculpts subcellular segregation of sensory inputs.

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.

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.

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.