ArticleNature communications2021
FoxG1 regulates the formation of cortical GABAergic circuit during an early postnatal critical period resulting in autism spectrum disorder-like phenotypes.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Efficacy and Safety of Stem Cell Therapy in Children With Autism Spectrum Disorders: A Systematic Review and Meta-Analysis.Frontiers in pediatrics · 2022Pooled it
- Article
- Review
- Hypoactivity, abnormal development of dendrites relevant to impaired synaptic transmission of calretinin-expressing interneurons in the medial prefrontal cortex underlies social deficits of mouse model in autism.Translational psychiatry · 2026Article
- Differential Neurodevelopmental Disruption by Bisphenol A (BPA) and Valproic Acid (VPA) in Human Forebrain Organoids.bioRxiv : the preprint server for biology · 2026Article
- Uncovering Hidden Phenotypes in NEX-Cre Mice: Behavioral and Cellular Alterations Demand Re-Evaluation of a Widely Used Transgenic Line.Journal of neurochemistry · 2026Article
- Article
- Early life shifts in cortical inhibitory-excitatory balance underlies sensitive periods and skill development.Frontiers in cellular neuroscience · 2026Article
- The lincRNA Pantr1 is a FOXG1 target gene conferring site-specific chromatin binding of FOXG1.Nucleic acids research · 2025Article
- Foxg1 gene mutation impairs auditory cortex response and reduces sound tolerance.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
- The patient-specific mouse model with Foxg1 frameshift mutation provides insights into the pathophysiology of FOXG1 syndrome.Nature communications · 2025Article
- Editorial: Cellular and molecular mechanisms that govern assembly, plasticity, and function of GABAergic inhibitory circuits in the mammalian brain.Frontiers in cellular neuroscience · 2025Article
- Neurosteroid withdrawal disrupts GABAergic system development in human cortical organoids: implications for preterm birth.Frontiers in cellular neuroscience · 2025Article
- GABA/Glutamate Neuron Differentiation Imbalance and Increased AKT/mTOR Signaling in CNTNAP2Biological psychiatry global open science · 2025Article
- PLP1-Targeting Antisense Oligonucleotides Improve FOXG1 Syndrome Mice.International journal of molecular sciences · 2024Article
- The postnatal injection of AAV9-FOXG1 rescues corpus callosum agenesis and other brain deficits in the mouse model of FOXG1 syndrome.Molecular therapy. Methods & clinical development · 2024Article
- Foxg1 regulates translation of neocortical neuronal genes, including the main NMDA receptor subunit gene, Grin1.BMC biology · 2024Article
- Foxg1 bimodally tunes L1-mRNA and -DNA dynamics in the developing murine neocortex.Development (Cambridge, England) · 2024Article
- FoxG1 as a Potential Therapeutic Target for Alzheimer's Disease: Modulating NLRP3 Inflammasome via AMPK/mTOR Autophagy Pathway.Cellular and molecular neurobiology · 2024Article
- Developmental trajectories of GABAergic cortical interneurons are sequentially modulated by dynamicProceedings of the National Academy of Sciences of the United States of America · 2024Article
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
Abstract
Abnormalities in GABAergic inhibitory circuits have been implicated in the aetiology of autism spectrum disorder (ASD). ASD is caused by genetic and environmental factors. Several genes have been associated with syndromic forms of ASD, including FOXG1. However, when and how dysregulation of FOXG1 can result in defects in inhibitory circuit development and ASD-like social impairments is unclear. Here, we show that increased or decreased FoxG1 expression in both excitatory and inhibitory neurons results in ASD-related circuit and social behavior deficits in our mouse models. We observe that the second postnatal week is the critical period when regulation of FoxG1 expression is required to prevent subsequent ASD-like social impairments. Transplantation of GABAergic precursor cells prior to this critical period and reduction in GABAergic tone via Gad2 mutation ameliorates and exacerbates circuit functionality and social behavioral defects, respectively. Our results provide mechanistic insight into the developmental timing of inhibitory circuit formation underlying ASD-like phenotypes in mouse models.
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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.