ArticleCell reports2022
Neural circuit pathology driven by Shank3 mutation disrupts social behaviors.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- ERK-dependent hyperexcitability of BLA neurons projecting to dCA3 underlies social dysfunction in a male mouse model of fragile X syndrome.EBioMedicine · 2026Article
- Subcortical Dendritic Scaffolding in Autism Spectrum Disorder: A Testable ANK2-SCN2A-SHANK Framework.International journal of molecular sciences · 2026Review
- δ-catenin haploinsufficiency is sufficient to alter behaviors and glutamatergic synapses in mice.Neuroscience · 2026Article
- Sex-dependent prediction of autism.Frontiers in genetics · 2026Article
- Sensory abnormalities in autism spectrum disorder and their in vitro modeling.Translational psychiatry · 2025Review
- Heightened empathic responses led by imbalanced cortico-amygdala circuit inbioRxiv : the preprint server for biology · 2025Article
- Early postnatal dysfunction of ACC PV interneurons in Shank3BMolecular psychiatry · 2025Article
- Closed-loop pathways associated with clinical symptoms in children with autism spectrum disorder: a complex network analysis.Quantitative imaging in medicine and surgery · 2025Article
- Brain circuits that regulate social behavior.Molecular psychiatry · 2025Review
- Restoration of excitation/inhibition balance enhances neuronal signal-to-noise ratio and rescues social deficits in autism-associatedbioRxiv : the preprint server for biology · 2025Article
- Endothelial SHANK3 regulates tight junctions in the neonatal mouse blood-brain barrier through β-Catenin signaling.Nature communications · 2025Article
- Restoration of nNOS Expression Rescues Autistic-Like Phenotypes Through Normalization of AMPA Receptor-Mediated Neurotransmission.Molecular neurobiology · 2024Article
- Scn2a insufficiency alters spontaneous neuronal CaiScience · 2023Article
- The PFC-LH-VTA pathway contributes to social deficits in IRSp53-mutant mice.Molecular psychiatry · 2023Article
- Social circuits and their dysfunction in autism spectrum disorder.Molecular psychiatry · 2023Review
- YBX1-Mediated DNA Methylation-Dependent SHANK3 Expression in PBMCs and Developing Cortical Interneurons in Schizophrenia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Maturation of a cortical-amygdala circuit limits sociability in male rats.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- Immune activation during pregnancy exacerbates ASD-related alterations in Shank3-deficient mice.Molecular autism · 2023Article
- Bridging the translational gap: what can synaptopathies tell us about autism?Frontiers in molecular neuroscience · 2023Review
- The role of the prefrontal cortex in social interactions of animal models and the implications for autism spectrum disorder.Frontiers in psychiatry · 2023Review
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Authors and funding
9 authors.
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Abstract
Dysfunctional sociability is a core symptom in autism spectrum disorder (ASD) that may arise from neural-network dysconnectivity between multiple brain regions. However, pathogenic neural-network mechanisms underlying social dysfunction are largely unknown. Here, we demonstrate that circuit-selective mutation (ctMUT) of ASD-risk Shank3 gene within a unidirectional projection from the prefrontal cortex to the basolateral amygdala alters spine morphology and excitatory-inhibitory balance of the circuit. Shank3 ctMUT mice show reduced sociability as well as elevated neural activity and its amplitude variability, which is consistent with the neuroimaging results from human ASD patients. Moreover, the circuit hyper-activity disrupts the temporal correlation of socially tuned neurons to the events of social interactions. Finally, optogenetic circuit activation in wild-type mice partially recapitulates the reduced sociability of Shank3 ctMUT mice, while circuit inhibition in Shank3 ctMUT mice partially rescues social behavior. Collectively, these results highlight a circuit-level pathogenic mechanism of Shank3 mutation that drives social dysfunction.
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