ArticleNature neuroscience2019
Anterior cingulate cortex dysfunction underlies social deficits in Shank3 mutant mice.
Article in Nature neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 172 papers, 3 of them syntheses that pooled it.
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Who cites it
172 citing papers in PubMed, 3 syntheses or guidelines pooled it, 285 citations in OpenAlex.
- Neurometabolite differences in Autism as assessed with Magnetic Resonance Spectroscopy: A systematic review and meta-analysis.Neuroscience and biobehavioral reviews · 2024Pooled it
- Systematic review and meta-analysis: multimodal functional and anatomical neural alterations in autism spectrum disorder.Molecular autism · 2024Pooled it
- Treatment Response of Transcranial Magnetic Stimulation in Intellectually Capable Youth and Young Adults with Autism Spectrum Disorder: A Systematic Review and Meta-Analysis.Neuropsychology review · 2023Pooled it
- Safety and target engagement of an oral small-molecule sequestrant in adolescents with autism spectrum disorder: an open-label phase 1b/2a trial.Nature medicine · 2022Trial
- A randomized controlled trial of intranasal oxytocin in Phelan-McDermid syndrome.Molecular autism · 2021Trial
- Effects of early-life tactile experience enrichment on autistic-like behaviors and synaptic alterations inFundamental research · 2026Article
- β-hydroxybutyrate restores social deficits by suppressing HDAC9 in the ACC of Shank3B-deficient mice.EMBO molecular medicine · 2026Article
- PACSIN2-mediated synaptic injury contributes to behavioral disorders caused by chronic stress.Acta pharmacologica Sinica · 2026Article
- Evaluation of Lead exposure's link to autism-like behavior and Shank 3 gene expression in C57BL/6J mice.The Journal of veterinary medical science · 2026Article
- Rannasangpei and its constituent crocin-1 ameliorate valproic acid-induced autism-like behaviors accompanied by reduced oxidative stress and neuroinflammation.Translational psychiatry · 2026Article
- Parallel anterior cingulate cortex pathways underlie dissociable social and attentional outputs.Science advances · 2026Article
- Genetic mutations and synaptic dysfunctions in social interaction disorders: insights from invertebrate models to humans.Metabolic brain disease · 2026Review
- Self-vocalizations activate the developing auditory cortex via an intracortical pathway.Science advances · 2026Article
- Anterior Cingulate Cortex Mediates State-Dependent Prioritization of Distressed Conspecifics.Brain sciences · 2026Article
- Lateral Habenula 5-HT₂A Receptors Mediate Social Deficits in a Valproic Acid-Induced Rodent Model of Autism Spectrum Disorder.Molecular neurobiology · 2026Article
- Olfactory Valence-Processing Deficits and Aberrant Brain Network Connectivity Underlie Social Dysfunction in Shank3Neuroscience bulletin · 2026Article
- Diverse Neuronal Activity in Barrel Cortex During Self-Grooming and Whisking in Mice.Neuroscience bulletin · 2026Article
- 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
- Article
- FOXG1 Hierarchically Shapes Synaptic Functions in Striatal iSPNs and Contributes to ASD Etiology.Neuroscience bulletin · 2026Article
112 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Social deficit is a core clinical feature of autism spectrum disorder (ASD) but the underlying neural mechanisms remain largely unclear. We demonstrate that structural and functional impairments occur in glutamatergic synapses in the pyramidal neurons of the anterior cingulate cortex (ACC) in mice with a mutation in Shank3, a high-confidence candidate ASD gene. Conditional knockout of Shank3 in the ACC was sufficient to generate excitatory synaptic dysfunction and social interaction deficits, whereas selective enhancement of ACC activity, restoration of SHANK3 expression in the ACC, or systemic administration of an α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor-positive modulator improved social behavior in Shank3 mutant mice. Our findings provide direct evidence for the notion that the ACC has a role in the regulation of social behavior in mice and indicate that ACC dysfunction may be involved in social impairments in ASD.
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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.