GluN2A expression levels and not GluN2 subtype-specific C terminal domain-driven events are the overriding factor in the developmental switch in NMDAR composition.
Homer1a may be a key neuroprotective endogenous molecule that protects against NMDA-induced neuronal injury by disassembling NR2B-PSD95-nNOS complexes and reducing the membrane distribution of NR2B.
Disrupting NR2B-Cdk5 interaction via a small interfering peptide (siP) increases NR2B surface levels facilitates synaptic transmission and improves memory formation in vivo.
Semi-quantitative analysis of RNA levels in FMRP immunoprecipitates showed that in the mouse brain mRNAs encoding PSD components such as Shank1 SAPAP1-3 PSD-95 and the glutamate receptor subunits NR1 and NR2B are associated with FMRP.
The NR2B subunit-containing N-methyl-D-aspartate (NMDA) receptors accumulate on the synaptic site and are responsible for synaptic function and plasticity in the amygdala.
Results identify the amino acid sequence HLFY as a signal necessary for the release of the assembled functional NMDA receptor complex from the endoplasmic reticulum.
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