ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2018
Adult
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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Who cites it
45 citing papers in PubMed, 79 citations in OpenAlex.
- Periodic and aperiodic contributions to EEG delta power are translatable and complementary Angelman syndrome biomarkers.Communications medicine · 2026Article
- Operant behavior is reliably impaired in a mouse model of Angelman syndrome.Research square · 2026Article
- UBE3A stabilization of β-catenin preserves synaptic proteins essential for motor and cognitive functions in Angelman Syndrome.Molecular autism · 2025Article
- Cortical layer-specific abnormalities in auditory responses in a mouse model of Fragile X Syndrome.Neurobiology of disease · 2025Article
- Deficiency of calretinin in prefrontal cortex causes behavioral deficits relevant to autism spectrum disorder in mice.Molecular brain · 2025Article
- Activity-dependent degradation of Kv4.2 contributes to synaptic plasticity and behavior in Angelman syndrome model mice.Cell reports · 2025Article
- Hyperexcitability and translational phenotypes in a preclinical mouse model of SYNGAP1-related intellectual disability.Translational psychiatry · 2024Article
- Hyperexcitability and translational phenotypes in a preclinical mouse model ofResearch square · 2024Article
- Regional and cellular organization of the autism-associated protein UBE3A/E6AP and its antisense transcript in the brain of the developing rhesus monkey.Frontiers in neuroanatomy · 2024Article
- Hyperexcitability and translational phenotypes in a preclinical model ofResearch square · 2023Article
- UBE3A expression during early postnatal brain development is required for proper dorsomedial striatal maturation.JCI insight · 2023Article
- Therapeutic strategies for autism: targeting three levels of the central dogma of molecular biology.Translational psychiatry · 2023Review
- Article
- Stem cell models of Angelman syndrome.Frontiers in cell and developmental biology · 2023Review
- The Hippocampal Response to Acute Corticosterone Elevation Is Altered in a Mouse Model for Angelman Syndrome.International journal of molecular sciences · 2022Article
- Acetate supplementation restores cognitive deficits caused by ARID1A haploinsufficiency in excitatory neurons.EMBO molecular medicine · 2022Article
- AdultiScience · 2022Article
- Development of prefrontal cortex.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022Review
- Dissociating motor impairment from five-choice serial reaction time task performance in a mouse model of Angelman syndrome.Frontiers in behavioral neuroscience · 2022Article
- Autism Spectrum Disorder Genes: Disease-Related Networks and Compensatory Strategies.Frontiers in molecular neuroscience · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
E3 ubiquitin ligase (UBE3A) levels in the brain need to be tightly regulated, as loss of functional UBE3A protein is responsible for the severe neurodevelopmental disorder Angelman syndrome (AS), whereas increased activity of UBE3A is associated with nonsyndromic autism. Given the role of mPFC in neurodevelopmental disorders including autism, we aimed to identify the functional changes resulting from loss of UBE3A in infralimbic and prelimbic mPFC areas in a mouse model of AS. Whole-cell recordings from layer 5 mPFC pyramidal neurons obtained in brain slices from adult mice of both sexes revealed that loss of UBE3A results in a strong decrease of spontaneous inhibitory transmission and increase of spontaneous excitatory transmission potentially leading to a marked excitation/inhibition imbalance. Additionally, we found that loss of UBE3A led to decreased excitability and increased threshold for action potential of layer 5 fast spiking interneurons without significantly affecting the excitability of pyramidal neurons. Because we previously showed that AS mouse behavioral phenotypes are reversible upon
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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.