ArticleMolecular psychiatry2021
Dysfunction of Trio GEF1 involves in excitatory/inhibitory imbalance and autism-like behaviors through regulation of interneuron migration.
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 21 papers.
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21 citing papers in PubMed, 36 citations in OpenAlex.
- 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
- MELK is Required for G2/M Phase Progression in Cortical Progenitors: Insights from Rare ASD-Associated Variants.Cellular and molecular neurobiology · 2026Article
- Aperiodic and periodic neural activity during sleep in autism spectrum disorders.BMC medicine · 2026Article
- Effects of gestational perfluorohexanesulfonic acid exposure at human realistic dose on social communication deficit in mouse offspring.EBioMedicine · 2026Article
- Astragaloside IV ameliorates autism-like behaviors in BTBR mice by modulating Camk2n2-dependent OXPHOS and neurotransmission in the mPFC.Journal of advanced research · 2025Article
- Deficiency of calretinin in prefrontal cortex causes behavioral deficits relevant to autism spectrum disorder in mice.Molecular brain · 2025Article
- Article
- Differential effects of left DLPFC anodal and cathodal tDCS interventions on the brain in children with autism: A randomized controlled trial.IBRO neuroscience reports · 2025Article
- Both GEF domains of the autism and developmental epileptic encephalopathy-associated Trio protein are required for proper tangential migration of GABAergic interneurons.Molecular psychiatry · 2025Article
- Prenatal Valproic Acid Exposure Impairs Offspring Cognition Through Disturbing Interneuron Development.CNS neuroscience & therapeutics · 2025Article
- Early postnatal exposure to bicuculline modulates E/I balance and induces ASD-like behavioral phenotypes in mice.Animal cells and systems · 2025Article
- Dentate Gyrus Morphogenesis is Regulated by an Autism Risk Gene Trio Function in Granule Cells.Neuroscience bulletin · 2025Article
- Common Genetic Variants inGenetics research · 2025Article
- Mechanisms of glutamate receptors hypofunction dependent synaptic transmission impairment in the hippocampus of schizophrenia susceptibility gene Opcml-deficient mouse model.Molecular brain · 2024Article
- Prenatal 1-Nitropyrene Exposure Causes Autism-Like Behavior Partially by Altering DNA Hydroxymethylation in Developing Brain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Deficiency of autism susceptibility gene Trio in cerebellar Purkinje cells leads to delayed motor impairments.Frontiers in psychiatry · 2024Article
- Rare genetic brain disorders with overlapping neurological and psychiatric phenotypes.Nature reviews. Neurology · 2024Review
- Maternal sevoflurane exposure increases the epilepsy susceptibility of adolescent offspring by interrupting interneuron development.BMC medicine · 2023Article
- Interneuron odyssey: molecular mechanisms of tangential migration.Frontiers in neural circuits · 2023Review
- Conditional knockout of ASK1 in microglia/macrophages attenuates epileptic seizures and long-term neurobehavioural comorbidities by modulating the inflammatory responses of microglia/macrophages.Journal of neuroinflammation · 2022Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism spectrum disorders (ASDs) are a group of highly inheritable neurodevelopmental disorders. Functional mutations in TRIO, especially in the GEF1 domain, are strongly implicated in ASDs, whereas the underlying neurobiological pathogenesis and molecular mechanisms remain to be clarified. Here we characterize the abnormal morphology and behavior of embryonic migratory interneurons (INs) upon Trio deficiency or GEF1 mutation in mice, which are mediated by the Trio GEF1-Rac1 activation and involved in SDF1α/CXCR4 signaling. In addition, the migration deficits are specifically associated with altered neural microcircuit, decreased inhibitory neurotransmission, and autism-like behaviors, which are reminiscent of some features observed in patients with ASDs. Furthermore, restoring the excitatory/inhibitory (E/I) imbalance via activation of GABA signaling rescues autism-like deficits. Our findings demonstrate a critical role of Trio GEF1 mediated signaling in IN migration and E/I balance, which are related to autism-related behavioral phenotypes.
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