ArticleMolecular psychiatry2021
Cell-type-specific synaptic imbalance and disrupted homeostatic plasticity in cortical circuits of ASD-associated Chd8 haploinsufficient mice.
Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 47 citations in OpenAlex.
- Homozygous CHD8 mutation intensifies ASD phenotypes and attenuates sex differences.Molecular psychiatry · 2026Article
- Autism subtypes identified using cross-species functional connectivity analyses.Nature neuroscience · 2026Article
- Transcriptomic and phenotypic convergence of neurodevelopmental disorder risk genes in vitro and in vivo.Nature neuroscience · 2026Article
- Knockdown of Ddx3x in mPFC induces autistic-like phenotype in mice via altered synaptic plasticity.Translational psychiatry · 2026Article
- Convergence and divergence of molecular mechanisms in Hebbian and homeostatic plasticity.Frontiers in synaptic neuroscience · 2026Review
- Cell-type-specific dysregulation of gene expression due to Chd8 haploinsufficiency during mouse cortical development.Cell genomics · 2025Article
- Multiple autism genes influence GABA neuron remodeling via distinct developmental trajectories.Genetics · 2025Article
- Persistent cortical excitatory neuron dysregulation in adultResearch square · 2025Article
- Dynamic convergence of neurodevelopmental disorder risk genes across neurodevelopment.bioRxiv : the preprint server for biology · 2025Article
- Multiple autism genes influence GABA neuron remodeling via distinct developmental trajectories.bioRxiv : the preprint server for biology · 2025Article
- Modular arrangement of synaptic and intrinsic homeostatic plasticity within visual cortical circuits.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Biological subtyping of autism via cross-species fMRI.bioRxiv : the preprint server for biology · 2025Article
- SINEUP RNA rescues molecular phenotypes associated with CHD8 suppression in autism spectrum disorder model systems.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Modular Arrangement of Synaptic and Intrinsic Homeostatic Plasticity within Visual Cortical Circuits.bioRxiv : the preprint server for biology · 2025Article
- The CHD Protein, Kismet, Restricts Synaptic BMP Signaling at Glutamatergic Synapses.Neuroscience insights · 2025Article
- Male-Dominant Effects of Chd8 Haploinsufficiency on Synaptic Phenotypes during Development in Mouse Prefrontal Cortex.ACS chemical neuroscience · 2024Article
- Etiologies underlying sex bias in autism spectrum disorder: a narrative review of preclinical rodent models.Ewha medical journal · 2024Review
- Neurodevelopmental functions of CHD8: new insights and questions.Biochemical Society transactions · 2024Review
- Deletion of the autism-related gene Chd8 alters activity-dependent transcriptional responses in mouse postmitotic neurons.Communications biology · 2023Article
- A synaptic molecular dependency network in knockdown of autism- and schizophrenia-associated genes revealed by multiplexed imaging.Cell reports · 2023Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Heterozygous mutation of chromodomain helicase DNA binding protein 8 (CHD8) is strongly associated with autism spectrum disorder (ASD) and results in dysregulated expression of neurodevelopmental and synaptic genes during brain development. To reveal how these changes affect ASD-associated cortical circuits, we studied synaptic transmission in the prefrontal cortex of a haploinsufficient Chd8 mouse model. We report profound alterations to both excitatory and inhibitory synaptic transmission onto deep layer projection neurons, resulting in a reduced excitatory:inhibitory balance, which were found to vary dynamically across neurodevelopment and result from distinct effects of reduced Chd8 expression within individual neuronal subtypes. These changes were associated with disrupted regulation of homeostatic plasticity mechanisms operating via spontaneous neurotransmission. These findings therefore directly implicate CHD8 mutation in the disruption of ASD-relevant circuits in the cortex.
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