ArticleThe Journal of pharmacology and experimental therapeutics2009
Expression of glycine-activated diheteromeric NR1/NR3 receptors in human embryonic kidney 293 cells Is NR1 splice variant-dependent.
Article in The Journal of pharmacology and experimental therapeutics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- The GluN3-containing NMDA receptors.Channels (Austin, Tex.) · 2025Review
- Allosteric modulation of GluN1/GluN3 NMDA receptors by GluN1-selective competitive antagonists.The Journal of general physiology · 2023Article
- Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels.Pharmacological reviews · 2021Review
- Conformational rearrangement of the NMDA receptor amino-terminal domain during activation and allosteric modulation.Nature communications · 2021Article
- Negative allosteric modulation of GluN1/GluN3 NMDA receptors.Neuropharmacology · 2020Article
- Site of Action of Brain Neurosteroid Pregnenolone Sulfate at the N-Methyl-D-Aspartate Receptor.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Structural features in the glycine-binding sites of the GluN1 and GluN3A subunits regulate the surface delivery of NMDA receptors.Scientific reports · 2019Article
- Unmasking GluN1/GluN3A excitatory glycine NMDA receptors.Nature communications · 2018Article
- Kinetic models for activation and modulation of NMDA receptor subtypes.Current opinion in physiology · 2018Article
- Article
- Residues in the GluN1 C-terminal domain control kinetics and pharmacology of GluN1/GluN3A N-methyl-d-aspartate receptors.Neuropharmacology · 2017Article
- Positive Modulatory Interactions of NMDA Receptor GluN1/2B Ligand Binding Domains Attenuate Antagonists Activity.Frontiers in pharmacology · 2017Article
- Protons Potentiate GluN1/GluN3A Currents by Attenuating Their Desensitisation.Scientific reports · 2016Article
- Block of NMDA receptor channels by endogenous neurosteroids: implications for the agonist induced conformational states of the channel vestibule.Scientific reports · 2015Article
- A naturally occurring null variant of the NMDA type glutamate receptor NR3B subunit is a risk factor of schizophrenia.PloS one · 2015Article
- Structure-based discovery of antagonists for GluN3-containing N-methyl-D-aspartate receptors.Neuropharmacology · 2013Article
- Moderate prenatal alcohol exposure reduces plasticity and alters NMDA receptor subunit composition in the dentate gyrus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Open-channel blockade is less effective on GluN3B than GluN3A subunit-containing NMDA receptors.European journal of pharmacology · 2012Article
- Distinct pharmacological and functional properties of NMDA receptors in mouse cortical astrocytes.British journal of pharmacology · 2011Article
- Potentiation of Glycine-Gated NR1/NR3A NMDA Receptors Relieves Ca-Dependent Outward Rectification.Frontiers in molecular neuroscience · 2010Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In oocytes, glycine activates receptors formed by diheteromeric combinations of N-methyl-d-aspartate (NMDA) NR1 and NR3 subunits. In contrast, functional receptors in mammalian cells require the simultaneous expression of NR1 and both NR3A and NR3B subunits. In vivo, NR3A and NR3B subunits show differential expression patterns and thus may not naturally form triheteromeric receptors. In this study, we examined whether NR1 splice variants play a role in allowing assembly of functional diheteromeric receptors in mammalian cells. Little current was found in human embryonic kidney 293 cells coexpressing either NR3A or NR3B and the NR1-1a splice variant. However, robust glycine-activated currents were generated in cells transfected with NR3(A or B) and either NR1-2a, NR1-3a, or NR1-4a, and current density was correlated with NR1 C-terminal length. Truncation of the NR1-1a C terminus modestly enhanced NR1-1a/NR3A currents, whereas only small increases were observed with mutations of C-terminal residues that control trafficking or phosphorylation. In contrast, large currents were observed when an extracellular phenylalanine in NR1-1a that influences glycine access was mutated to alanine. A separate mutation in NR1-1a that disrupts glycine binding did not generate responses in NR1-1a/NR3A receptors alone, but it produced a greater than 30-fold potentiation of currents during coapplication of glycine and the glycine antagonist 7-chlorokynurenic acid. Finally, transfection of cells with the NR1-4a subunit along with NR2 and NR3 subunits resulted in the expression of both NR1/NR3 receptors and conventional NMDA receptor currents. These results indicate a prominent role for NR1 splice variants in the functional expression of NR1/NR3 receptors in mammalian cells.
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