ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Fragile X protein FMRP is required for homeostatic plasticity and regulation of synaptic strength by retinoic acid.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers, 1 of them a synthesis that pooled it.
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Who cites it
122 citing papers in PubMed, 1 synthesis or guideline pooled it, 187 citations in OpenAlex.
- The Synaptic Scaling Literature: A Systematic Review of Methodologies and Quality of Reporting.Frontiers in cellular neuroscience · 2020Pooled it
- Telehealth-enabled behavioral treatment for problem behaviors in boys with fragile X syndrome: a randomized controlled trial.Journal of neurodevelopmental disorders · 2020Trial
- Discourse Marker Use in Mothers of Autistic Individuals and FMR1 Premutation Carriers.Journal of autism and developmental disorders · 2026Article
- Memory processing in neurodevelopmental disorders: linking behavioral, circuits, and molecular scales.Frontiers in cellular neuroscience · 2026Review
- Convergence and divergence of molecular mechanisms in Hebbian and homeostatic plasticity.Frontiers in synaptic neuroscience · 2026Review
- Article
- Division of labor among H3K4 methyltransferases defines distinct facets of homeostatic plasticity.Cell reports · 2025Article
- Impairment in the homeostatic recruitment of layer 5/6 neurons following whisker stimulation in Fmr1 KO mice.Neurobiology of disease · 2025Article
- Retinoic acid-mediated homeostatic plasticity in the nucleus accumbens core contributes to incubation of cocaine craving.Psychopharmacology · 2024Article
- Differential Effects of a Behavioral Treatment Probe on Social Gaze Behavior in Fragile X Syndrome and Non-Syndromic Autism Spectrum Disorder.Journal of autism and developmental disorders · 2024Article
- TCF4 Mutations Disrupt Synaptic Function Through Dysregulation of RIMBP2 in Patient-Derived Cortical Neurons.Biological psychiatry · 2024Article
- mGluR7 allosteric modulator AMN082 corrects protein synthesis and pathological phenotypes in FXS.EMBO molecular medicine · 2024Article
- Diverging from the Norm: Reevaluating What Miniature Excitatory Postsynaptic Currents Tell Us about Homeostatic Synaptic Plasticity.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- Roles of AMPA receptors in social behaviors.Frontiers in synaptic neuroscience · 2024Review
- Retinoic acid modulation of granule cell activity and spatial discrimination in the adult hippocampus.Frontiers in cellular neuroscience · 2024Article
- Synaptic scaling of corticostriatal circuits underlies hyperactivity in GABA Transporter-1 deficient mice.iScience · 2023Article
- Article
- TCF4 mutations disrupt synaptic function through dysregulation of RIMBP2 in patient-derived cortical neurons.bioRxiv : the preprint server for biology · 2023Article
- Circuit-level theories for sensory dysfunction in autism: convergence across mouse models.Frontiers in neurology · 2023Review
- The effect of single-cell knockout of Fragile X Messenger Ribonucleoprotein on synaptic structural plasticity.Frontiers in synaptic neuroscience · 2023Article
62 more citing papers are in PubMed but not listed here.
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2 authors at 1 institution in 2 countries.
Funding
Abstract
Homeostatic synaptic plasticity adjusts the strength of synapses during global changes in neural activity, thereby stabilizing the overall activity of neural networks. Suppression of synaptic activity increases synaptic strength by inducing synthesis of retinoic acid (RA), which activates postsynaptic synthesis of AMPA-type glutamate receptors (AMPARs) in dendrites and promotes synaptic insertion of newly synthesized AMPARs. Here, we show that fragile X mental retardation protein (FMRP), an RNA-binding protein that regulates dendritic protein synthesis, is essential for increases in synaptic strength induced by RA or by blockade of neural activity in the mouse hippocampus. Although activity-dependent RA synthesis is maintained in Fmr1 knock-out neurons, RA-dependent dendritic translation of GluR1-type AMPA receptors is impaired. Intriguingly, FMRP is only required for the form of homeostatic plasticity that is dependent on both RA signaling and local protein synthesis. Postsynaptic expression of wild-type or mutant FMRP(I304N) in knock-out neurons reduced the total, surface, and synaptic levels of AMPARs, implying a role for FMRP in regulating AMPAR abundance. Expression of FMRP lacking the RGG box RNA-binding domain had no effect on AMPAR levels. Importantly, postsynaptic expression of wild-type FMRP, but not FMRP(I304N) or FMRPΔRGG, restored synaptic scaling when expressed in knock-out neurons. Together, these findings identify an unanticipated role for FMRP in regulating homeostatic synaptic plasticity downstream of RA. Our results raise the possibility that at least some of the symptoms of fragile X syndrome reflect impaired homeostatic plasticity and impaired RA signaling.
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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.