ArticleNature communications2017
Altered surface mGluR5 dynamics provoke synaptic NMDAR dysfunction and cognitive defects in Fmr1 knockout mice.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 94 citations in OpenAlex.
- Region- and cell type-specific changes in gene expression in the cerebellum after classical fear conditioning.Communications biology · 2026Article
- Enhanced CB1 receptor function in GABAergic neurons mediates hyperexcitability and impaired sensory-driven synchrony of cortical circuits in Fragile X Syndrome model mice.Molecular psychiatry · 2026Article
- Glutamate Metabotropic Receptors-Linked Postsynaptic Density Proteins: An Emergent Hub for Antipsychotics' Regulation of Synaptic Plasticity and Metaplasticity.Biomolecules · 2026Review
- Unraveling mGluR5 dysfunction in autism spectrum disorder: a multi-level analysis of genetic, molecular, and neurobiological mechanisms.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Review
- Aberrant hippocampal gamma oscillations in a mouse model of fragile X syndrome: insights from in vitro slice models.Molecular autism · 2025Article
- Conditional mGluR5 knockout in glutamatergic pathways disrupts the development of excitatory synaptic transmission onto mouse MNTB neurons.Journal of neurophysiology · 2025Article
- Spontaneous glutamate release activates mGluR signaling to drive rapid antidepressant responses.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Therapeutic Effects of Pharmacological Modulation of Serotonin Brain System in Human Patients and Animal Models of Fragile X Syndrome.International journal of molecular sciences · 2025Review
- Anti-metabotropic glutamate receptor 5 coexistent anti-N-methyl-D-aspartate receptor encephalitis: a case report and literature review.Frontiers in immunology · 2025Review
- Aberrant encoding of event saliency in the orbitofrontal cortex following loss of the psychiatric-associated circular RNA, circHomer1.Translational psychiatry · 2024Article
- Article
- Nanoscale Reorganization of Glutamate Receptors Underlies Synaptic Plasticity and Pathology.Neuroscience bulletin · 2024Review
- Parvalbumin interneuron activity in autism underlies susceptibility to PTSD-like memory formation.iScience · 2024Article
- SRC family kinase inhibition rescues molecular and behavioral phenotypes, but not protein interaction network dynamics, in a mouse model of Fragile X syndrome.Molecular psychiatry · 2024Article
- Proteomics insights into fragile X syndrome: Unraveling molecular mechanisms and therapeutic avenues.Neurobiology of disease · 2024Review
- Astroglial Kir4.1 potassium channel deficit drives neuronal hyperexcitability and behavioral defects in Fragile X syndrome mouse model.Nature communications · 2024Article
- Altered brain serotonin 5-HTNeuropharmacology · 2024Article
- The Impact of Genetics on Cognition: Insights into Cognitive Disorders and Single Nucleotide Polymorphisms.Journal of personalized medicine · 2024Article
- mGluR5 PAMs rescue cortical and behavioural defects in a mouse model of CDKL5 deficiency disorder.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
Corrections and comments
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Authors and funding
18 authors at 8 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabotropic glutamate receptor subtype 5 (mGluR5) is crucially implicated in the pathophysiology of Fragile X Syndrome (FXS); however, its dysfunction at the sub-cellular level, and related synaptic and cognitive phenotypes are unexplored. Here, we probed the consequences of mGluR5/Homer scaffold disruption for mGluR5 cell-surface mobility, synaptic N-methyl-D-aspartate receptor (NMDAR) function, and behavioral phenotypes in the second-generation Fmr1 knockout (KO) mouse. Using single-molecule tracking, we found that mGluR5 was significantly more mobile at synapses in hippocampal Fmr1 KO neurons, causing an increased synaptic surface co-clustering of mGluR5 and NMDAR. This correlated with a reduced amplitude of synaptic NMDAR currents, a lack of their mGluR5-activated long-term depression, and NMDAR/hippocampus dependent cognitive deficits. These synaptic and behavioral phenomena were reversed by knocking down Homer1a in Fmr1 KO mice. Our study provides a mechanistic link between changes of mGluR5 dynamics and pathological phenotypes of FXS, unveiling novel targets for mGluR5-based therapeutics.
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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.