ArticleFrontiers in synaptic neuroscience2021
GluN2D NMDA Receptors Gate Fear Extinction Learning and Interneuron Plasticity.
Article in Frontiers in synaptic neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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
18 citing papers in PubMed, 22 citations in OpenAlex.
- GluN2D NMDA Receptors: Bridging Physiology and Pathology.Biological psychiatry · 2026Review
- Heterosynaptic NMDA receptor plasticity in hippocampal dentate granule cells.Frontiers in synaptic neuroscience · 2026Article
- Enhancement of hippocampal interneuron excitability by NMDA receptor positive allosteric modulation.The Journal of physiology · 2025Article
- Chronic postoperative pain induces contextual fear extinction dysfunction through hippocampal NMDAR/BDNF/TrkB signaling pathway in mice.Translational psychiatry · 2025Article
- Emotional stress increases GluA2 expression and potentiates fear memory via adenylyl cyclase 5.Cell reports · 2025Article
- Systemic corticosterone enhances fear memory extinction in rats: Involvement of the infralimbic medial prefrontal cortex GABABrain and behavior · 2024Article
- Intrinsic plasticity of Purkinje cell serves homeostatic regulation of fear memory.Molecular psychiatry · 2024Article
- Therapeutic potential of N-methyl-D-aspartate receptor modulators in psychiatry.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Review
- Neuropharmacological Modulation of N-methyl-D-aspartate, Noradrenaline and Endocannabinoid Receptors in Fear Extinction Learning: Synaptic Transmission and Plasticity.International journal of molecular sciences · 2023Review
- GluN2D expression is regulated by restraint stress and supports active stress coping bouts.Neuropharmacology · 2023Article
- The cerebellum and fear extinction: evidence from rodent and human studies.Frontiers in systems neuroscience · 2023Review
- Cerebellar contributions to fear-based emotional processing: relevance to understanding the neural circuits involved in autism.Frontiers in systems neuroscience · 2023Review
- Esmethadone (REL-1017) and Other Uncompetitive NMDAR Channel Blockers May Improve Mood Disorders via Modulation of Synaptic Kinase-Mediated Signaling.International journal of molecular sciences · 2022Article
- Spider Neurotoxins as Modulators of NMDA Receptor Signaling.Neuromolecular medicine · 2022Review
- Cerebellar Circuits for Classical Fear Conditioning.Frontiers in cellular neuroscience · 2022Review
- An integrated cytokine and kynurenine network as the basis of neuroimmune communication.Frontiers in neuroscience · 2022Review
- Multiple roles of GluN2D-containing NMDA receptors in short-term potentiation and long-term potentiation in mouse hippocampal slices.Neuropharmacology · 2021Article
- Roles of N-Methyl-D-Aspartate Receptors (NMDARs) in Epilepsy.Frontiers in molecular neuroscience · 2021Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The cerebellum is critically involved in the formation of associative fear memory and in subsequent extinction learning. Fear conditioning is associated with a long-term potentiation at both excitatory and inhibitory synapses onto Purkinje cells. We therefore tested whether fear conditioning unmasks novel forms of synaptic plasticity, which enable subsequent extinction learning to reset cerebellar circuitry. We found that fear learning enhanced GABA release from molecular layer interneurons and this was reversed after fear extinction learning. Importantly an extinction-like stimulation of parallel fibers after fear learning is sufficient to induce a lasting decrease in inhibitory transmission (I-LTD
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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.