ArticleeNeuro
Contribution of NMDA Receptors to Synaptic Function in Rat Hippocampal Interneurons.
Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Inhibition of GluN2B-containing N-methyl-D-aspartate receptors by radiprodil.Brain : a journal of neurology · 2026Article
- Enhancement of hippocampal interneuron excitability by NMDA receptor positive allosteric modulation.The Journal of physiology · 2025Article
- A deep learning pipeline for accurate and automated restoration, segmentation, and quantification of dendritic spines.Cell reports methods · 2025Article
- Experimentally Constrained Mechanistic and Data-Driven Models for Simulating NMDA Receptor Dynamics.Biomedicines · 2025Article
- Selective enhancement of the interneuron network and gamma-band power via GluN2C/GluN2D NMDA receptor potentiation.The Journal of physiology · 2025Article
- Activation of GluN2D-containing NMDA receptors promotes development of axons and axon-carrying dendrites of cortical interneurons.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
- Absence of GluN2A in hippocampal CA1 neurons leads to altered dendritic structure and reduced frequency of miniature excitatory synaptic events.Brain communications · 2025Article
- Selective Cell-Surface Expression of Triheteromeric NMDA Receptors.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Loss of Grin2a causes a transient delay in the electrophysiological maturation of hippocampal parvalbumin interneurons.Communications biology · 2023Article
- Functional effects of disease-associated variants reveal that the S1-M1 linker of the NMDA receptor critically controls channel opening.Cellular and molecular life sciences : CMLS · 2023Article
- GluN2D expression is regulated by restraint stress and supports active stress coping bouts.Neuropharmacology · 2023Article
- Bidirectional plasticity of GABAergic tonic inhibition in hippocampal somatostatin- and parvalbumin-containing interneurons.Frontiers in cellular neuroscience · 2023Article
- Different modes of synaptic and extrasynaptic NMDA receptor alteration in the hippocampus of P301S tau transgenic mice.Brain pathology (Zurich, Switzerland) · 2023Article
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- Dose-dependent suppression of hippocampal contextual memory formation, place cells, and spatial engrams by the NMDAR antagonist (R)-CPP.Neuropharmacology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The ability of neurons to produce behaviorally relevant activity in the absence of pathology relies on the fine balance of synaptic inhibition to excitation. In the hippocampal CA1 microcircuit, this balance is maintained by a diverse population of inhibitory interneurons that receive largely similar glutamatergic afferents as their target pyramidal cells, with EPSCs generated by both AMPA receptors (AMPARs) and NMDA receptors (NMDARs). In this study, we take advantage of a recently generated GluN2A-null rat model to assess the contribution of GluN2A subunits to glutamatergic synaptic currents in three subclasses of interneuron found in the CA1 region of the hippocampus. For both parvalbumin-positive and somatostatin-positive interneurons, the GluN2A subunit is expressed at glutamatergic synapses and contributes to the EPSC. In contrast, in cholecystokinin (CCK)-positive interneurons, the contribution of GluN2A to the EPSC is negligible. Furthermore, synaptic potentiation at glutamatergic synapses on CCK-positive interneurons does not require the activation of GluN2A-containing NMDARs but does rely on the activation of NMDARs containing GluN2B and GluN2D subunits.
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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.