ArticleNeuron2014
Distinct functional and pharmacological properties of Triheteromeric GluN1/GluN2A/GluN2B NMDA receptors.
Article in Neuron, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 201 papers.
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Who cites it
201 citing papers in PubMed, 300 citations in OpenAlex.
- CaMKII monomers are sufficient for GluN2B binding, co-condensation, and synaptic potentiation.Molecular cell · 2026Article
- GluN2D NMDA Receptors: Bridging Physiology and Pathology.Biological psychiatry · 2026Review
- Cryo-EM structures of apo, agonist- and antagonist-bound heteromeric kainate receptors.Science advances · 2026Article
- Identification of a Class of Novel, Selective, Structurally Distinct GluN2A Negative Allosteric Modulators Through Virtual Screening.ChemMedChem · 2026Article
- Article
- State-specific inhibition of NMDA receptors by memantine provides insight into NMDAR channel blocker tolerability.Science advances · 2026Article
- Article
- Inhibition of GluN2B-containing N-methyl-D-aspartate receptors by radiprodil.Brain : a journal of neurology · 2026Article
- UCM-A86 is a selective positive allosteric modulator of GluN1/GluN3 NMDA receptors.Molecular pharmacology · 2026Article
- Emerging Roles of GluN3B NMDA Receptor Subunit in the Central Nervous System.Neuroscience bulletin · 2026Review
- Mice carrying a GluN2B protein-truncating variant have altered NMDA receptor subunit composition and their behavior recapitulates patient phenotypes.Cellular and molecular life sciences : CMLS · 2026Article
- Novel binding mode for negative allosteric NMDA receptor modulators.The Journal of general physiology · 2026Article
- New advances in small molecule drugs targeting NMDA receptors.Acta pharmacologica Sinica · 2026Review
- GluN2A-NMDA receptor inhibition disinhibits the prefrontal cortex, reduces forced swim immobility, and impairs sensorimotor gating.Acta pharmacologica Sinica · 2026Article
- UCM-A86 is a selective positive allosteric modulator of GluN1/GluN3 NMDA receptors.bioRxiv : the preprint server for biology · 2025Article
- Enhancement of hippocampal interneuron excitability by NMDA receptor positive allosteric modulation.The Journal of physiology · 2025Article
- Disruption ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Trans-synaptic molecular context of NMDA receptor nanodomains.Nature communications · 2025Article
- Optochemical profiling of NMDAR molecular diversity at synaptic and extrasynaptic sites.The EMBO journal · 2025Article
- Selective enhancement of the interneuron network and gamma-band power via GluN2C/GluN2D NMDA receptor potentiation.The Journal of physiology · 2025Article
141 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
NMDA receptors are tetrameric ligand-gated ion channels comprised of GluN1, GluN2, and GluN3 subunits. Two different GluN2 subunits have been identified in most NMDA receptor-expressing cells, and the majority of native receptors are triheteromers containing two GluN1 and two different GluN2. In contrast to diheteromeric NMDA receptors, little is known about the function of triheteromers. We developed a method to provide selective cell-surface expression of recombinant GluN1/GluN2A/GluN2B triheteromers and compared properties of these receptors with those of GluN1/GluN2A and GluN1/GluN2B diheteromers. We show that glutamate deactivation of triheteromers is distinct from those of GluN1/GluN2A and GluN1/GluN2B and reveal modulation of triheteromers by subunit-selective antagonists ifenprodil, CP-101,606, TCN-201, and extracellular Zn(2+). Furthermore, kinetic measurements suggest variation in the ifenprodil binding site of triheteromers compared to GluN1/GluN2B diheteromers. This work provides insight into the distinct properties of GluN1/GluN2A/GluN2B triheteromers, which are presumably the most abundant NMDA receptors in the adult forebrain.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.