ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2014
Potentiation of GluN2C/D NMDA receptor subtypes in the amygdala facilitates the retention of fear and extinction learning in mice.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
35 citing papers in PubMed, 54 citations in OpenAlex.
- d-Cycloserine augmentation of cognitive remediation in schizophrenia.Schizophrenia research · 2014Trial
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- Therapeutic potential of N-methyl-D-aspartate receptor modulators in psychiatry.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Review
- Treatment of Posttraumatic Stress Disorder: A State-of-the-art Review.Current neuropharmacology · 2024Review
- Discovery of (Frontiers in chemistry · 2022Article
- Astrocytic NMDA Receptors in the Basolateral Amygdala Contribute to Facilitation of Fear Extinction.The international journal of neuropsychopharmacology · 2021Article
- Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels.Pharmacological reviews · 2021Review
- NMDA GluN2C/2D receptors contribute to synaptic regulation and plasticity in the anterior cingulate cortex of adult mice.Molecular brain · 2021Article
- NMDA Receptors Require Multiple Pre-opening Gating Steps for Efficient Synaptic Activity.Neuron · 2021Article
- GluN2D NMDA Receptors Gate Fear Extinction Learning and Interneuron Plasticity.Frontiers in synaptic neuroscience · 2021Article
- Discovery of Dihydropyrrolo[1,2-Journal of medicinal chemistry · 2020Article
- Differential effect of NMDA receptor GluN2C and GluN2D subunit ablation on behavior and channel blocker-induced schizophrenia phenotypes.Scientific reports · 2019Article
- N-Methyl D-aspartate receptor subunit signaling in fear extinction.Psychopharmacology · 2019Review
- Article
- A Novel Negative Allosteric Modulator Selective for GluN2C/2D-Containing NMDA Receptors Inhibits Synaptic Transmission in Hippocampal Interneurons.ACS chemical neuroscience · 2018Article
- The Bioactive Protein-Ligand Conformation of GluN2C-Selective Positive Allosteric Modulators Bound to the NMDA Receptor.Molecular pharmacology · 2018Article
- CIQ, a positive allosteric modulator of GluN2C/D-containing N-methyl-d-aspartate receptors, rescues striatal synaptic plasticity deficit in a mouse model of Parkinson's disease.CNS neuroscience & therapeutics · 2018Article
- How does binding of agonist ligands control intrinsic molecular dynamics in human NMDA receptors?PloS one · 2018Article
- Glutamatergic regulation of cognition and functional brain connectivity: insights from pharmacological, genetic and translational schizophrenia research.British journal of pharmacology · 2017Review
- Identification of AICP as a GluN2C-SelectiveMolecular pharmacology · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
NMDA receptors are glutamate receptor ion channels that contribute to synaptic plasticity and are important for many forms of learning and memory. In the amygdala, NMDA receptors are critical for the acquisition, retention, and extinction of classically conditioned fear responses. Although the GluN2B subunit has been implicated in both the acquisition and extinction of conditioned fear, GluN2C-knockout mice show reduced conditioned fear responses. Moreover, D-cycloserine (DCS), which facilitates fear extinction, selectively enhances the activity of GluN2C-containing NMDA receptors. To further define the contribution of GluN2C receptors to fear learning, we infused the GluN2C/GluN2D-selective potentiator CIQ bilaterally into the basolateral amygdala (3, 10, or 30 μg/side) following either fear conditioning or fear extinction training. CIQ both increased the expression of conditioned fear 24 h later and enhanced the extinction of the previously conditioned fear response. These results support a critical role for GluN2C receptors in the amygdala in the consolidation of learned fear responses and suggest that increased activity of GluN2C receptors may underlie the therapeutic actions of DCS.
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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.