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.
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.
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 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.
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.
The APP intracellular domain (AICD) physiologically regulates synaptic GluN2B-containing NMDA receptor current, a process that could contribute to pathological Alzheimer's disease-related synaptic failure upon increase of AICD levels in adult neurons.
A protein called RNF10 relays messages from synapses to neuron cell nuclei, and is responsible for long-lasting modifications of dendritic spines as observed after activation of synaptic glutamate receptors.
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.
