ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Homer protein-metabotropic glutamate receptor binding regulates endocannabinoid signaling and affects hyperexcitability in a mouse model of fragile X syndrome.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- 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
- Endocannabinoids at the synapse and beyond: implications for neuropsychiatric disease pathophysiology and treatment.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Review
- Review
- Neural Mechanisms Underlying Repetitive Behaviors in Rodent Models of Autism Spectrum Disorders.Frontiers in cellular neuroscience · 2020Review
- Of Men and Mice: Modeling the Fragile X Syndrome.Frontiers in molecular neuroscience · 2018Article
- Altered surface mGluR5 dynamics provoke synaptic NMDAR dysfunction and cognitive defects in Fmr1 knockout mice.Nature communications · 2017Article
- Hippocampal GABAergic Inhibitory Interneurons.Physiological reviews · 2017Review
- Synaptic functions of endocannabinoid signaling in health and disease.Neuropharmacology · 2017Review
- The DLGAP family: neuronal expression, function and role in brain disorders.Molecular brain · 2017Review
- Neurophysiology of space travel: energetic solar particles cause cell type-specific plasticity of neurotransmission.Brain structure & function · 2017Article
- Fragile X targeted pharmacotherapy: lessons learned and future directions.Journal of neurodevelopmental disorders · 2017Review
- Article
- Increased Persistent Sodium Current Causes Neuronal Hyperexcitability in the Entorhinal Cortex of Fmr1 Knockout Mice.Cell reports · 2016Article
- Orchestrated activation of mGluR5 and CB1 promotes neuroprotection.Molecular brain · 2016Article
- The Tau/A152T mutation, a risk factor for frontotemporal-spectrum disorders, leads to NR2B receptor-mediated excitotoxicity.EMBO reports · 2016Article
- Metabotropic Glutamate Receptors and Interacting Proteins in Epileptogenesis.Current neuropharmacology · 2016Review
- Elevated CaMKIIα and Hyperphosphorylation of Homer Mediate Circuit Dysfunction in a Fragile X Syndrome Mouse Model.Cell reports · 2015Article
- The endocannabinoid system in guarding against fear, anxiety and stress.Nature reviews. Neuroscience · 2015Review
- Dysregulation and restoration of translational homeostasis in fragile X syndrome.Nature reviews. Neuroscience · 2015Review
- Endocannabinoid-mediated improvement on a test of aversive memory in a mouse model of fragile X syndrome.Behavioural brain research · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
The Fmr1 knock-out mouse model of fragile X syndrome (Fmr1(-/y)) has an epileptogenic phenotype that is triggered by group I metabotropic glutamate receptor (mGluR) activation. We found that a membrane-permeable peptide that disrupts mGluR5 interactions with long-form Homers enhanced mGluR-induced epileptiform burst firing in wild-type (WT) animals, replicating the early stages of hyperexcitability in Fmr1(-/y). The peptide enhanced mGluR-evoked endocannabinoid (eCB)-mediated suppression of inhibitory synapses, decreased it at excitatory synapses in WTs, but had no effect on eCB actions in Fmr1(-/y). At a low concentration, the mGluR agonist did not generate eCBs at excitatory synapses but nevertheless induced burst firing in both Fmr1(-/y) and peptide-treated WT slices. This burst firing was suppressed by a cannabinoid receptor antagonist. We suggest that integrity of Homer scaffolds is essential for normal mGluR-eCB functioning and that aberrant eCB signaling resulting from disturbances of this molecular structure contributes to the epileptic phenotype of Fmr1(-/y).
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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.