ArticleProceedings of the National Academy of Sciences of the United States of America2010
Genomic imprinting of experience-dependent cortical plasticity by the ubiquitin ligase gene Ube3a.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
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Who cites it
95 citing papers in PubMed, 149 citations in OpenAlex.
- Memory processing in neurodevelopmental disorders: linking behavioral, circuits, and molecular scales.Frontiers in cellular neuroscience · 2026Review
- Environmental context modulates sociability in ube3a zebrafish mutants via alterations in sensory pathways.Molecular psychiatry · 2026Article
- Age-Dependent Process Governs Executive Function Disability in Autistic Children.Journal of autism and developmental disorders · 2025Article
- Alterations of synaptic plasticity in Angelman syndrome model mice are rescued by 5-HT7R stimulation.Progress in neurobiology · 2024Article
- UBE3A: The Role in Autism Spectrum Disorders (ASDs) and a Potential Candidate for Biomarker Studies and Designing Therapeutic Strategies.Diseases (Basel, Switzerland) · 2023Review
- Article
- An alternative splicing hypothesis for neuropathology of schizophrenia: evidence from studies on historical candidate genes and multi-omics data.Molecular psychiatry · 2022Review
- Article
- Insulin-like growth factor-2 does not improve behavioral deficits in mouse and rat models of Angelman Syndrome.Molecular autism · 2021Article
- Historical perspective and progress on protein ubiquitination at glutamatergic synapses.Neuropharmacology · 2021Review
- Angelman Syndrome and Angelman-like Syndromes Share the Same Calcium-Related Gene Signatures.International journal of molecular sciences · 2021Article
- Emerging Gene and Small Molecule Therapies for the Neurodevelopmental Disorder Angelman Syndrome.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- The role of GABAergic signalling in neurodevelopmental disorders.Nature reviews. Neuroscience · 2021Review
- Evaluation of UBE3A antibodies in mice and human cerebral organoids.Scientific reports · 2021Article
- Novel Therapeutic Approach for Excitatory/Inhibitory Imbalance in Neurodevelopmental and Neurodegenerative Diseases.Annual review of pharmacology and toxicology · 2021Review
- A Practical Guide to SparseFrontiers in neuroscience · 2021Article
- Communication-related assessments in an Angelman syndrome mouse model.Brain and behavior · 2021Article
- Control of cortical synapse development and plasticity by MET receptor tyrosine kinase, a genetic risk factor for autism.Journal of neuroscience research · 2020Review
- An Unbiased Drug Screen for Seizure Suppressors in Duplication 15q Syndrome Reveals 5-HTBiological psychiatry · 2020Article
- Deficits in higher visual area representations in a mouse model of Angelman syndrome.Journal of neurodevelopmental disorders · 2020Article
35 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
A defect in the maternal copy of a ubiqutin ligase gene Ube3a can produce a neurodevelopmental defect in human children known as Angelman syndrome. We investigated the role of the maternally expressed Ube3a gene in experience-dependent development and plasticity of the mouse visual system. As demonstrated by optical imaging, rapid ocular dominance (OD) plasticity after brief monocular deprivation (MD) was severely impaired during the critical period (CP) in the visual cortex (VC) of Ube3a maternal-deficient (m-/p+) mice. Prolonged MD elicited significant plasticity in m-/p+ mice that never matched the level seen in control animals. In older animals after the CP, 7-day MD elicited mild OD shifts in both control and m-/p+ mice; however, the OD shifts in m-/p+ mice lacked the strengthening of visual responses to the two eyes characteristic of normal adult plasticity. Anatomic effects of the maternal deficiency include reduced spine density on basal, but not apical, dendrites of pyramidal neurons in the binocular region of the VC. Imprinting of Ube3a expression was not fully established in the early postnatal period, consistent with the normal development of cortical retinotopy and visual acuity that we observed in m-/p+ mice, but was fully established by the onset of the CP. These results demonstrate that paternal and maternal genomes are not functionally equivalent for cortical plasticity, and that maternally expressed Ube3a is required for normal experience-dependent modification of cortical circuits during and after the CP.
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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.