ArticleNature communications2020
Autism spectrum disorder-like behavior caused by reduced excitatory synaptic transmission in pyramidal neurons of mouse prefrontal cortex.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
94 citing papers in PubMed, 1 synthesis or guideline pooled it, 148 citations in OpenAlex.
- Aberrant IL-17 Levels in Rodent Models of Autism Spectrum Disorder: A Systematic Review.Frontiers in immunology · 2022Pooled it
- An antioxidant therapy elicits distinct transcriptome responses in 22q11-deleted upper layer cortical projection neurons.Disease models & mechanisms · 2026Article
- Impaired behavioral inhibition in Fmr1 KO mice is linked to disrupted visual cortex theta oscillations.Cell reports · 2026Article
- The role of astrocytes in autism spectrum disorder and associated syndromes: Evidence, animal models, mechanisms, and therapeutic potential.Zoological research · 2026Review
- Phosphoproteomic profiling reveals reversal of dysregulated kinase signaling by nitric oxide inhibition in the Shank3 mouse model of autism.Scientific reports · 2026Article
- Parental gut microbiota dysbiosis is associated with cross-generationally shared DNA methylation patterns and autism-like behaviors in offspring.NPJ biofilms and microbiomes · 2026Article
- Mercury-induced excitotoxicity in autism spectrum disorder: disruption of glutamatergic homeostasis and the therapeutic role of the selenium-glutathione axis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- The development of positron emission tomography (PET) tracer for glutamate AMPA receptors and its application to human biology and clinics.Psychiatry and clinical neurosciences · 2026Review
- FOXG1 Hierarchically Shapes Synaptic Functions in Striatal iSPNs and Contributes to ASD Etiology.Neuroscience bulletin · 2026Article
- Dysregulated GluA2-Y876 phosphorylation contributes to loss of synaptic upscaling in GRIP1 mutant mice with reduced sociability and increased repetitive behavior.Molecular psychiatry · 2026Article
- Disrupted Development of the mPFC-Thalamic Circuit in Shank3Molecular psychiatry · 2026Article
- Mll5 haploinsufficiency attenuates microglial phagocytosis through dysregulated TREM2-SGK3-GSK3β signaling and recapitulates ASD-like behaviors in mice.Nature communications · 2026Article
- Sh3rf3 Deficiency drives autism-like behaviors via presynaptic dysfunction in mice.Molecular psychiatry · 2026Article
- Repeated Stress Escalates Aggression and Activity in Fronto-Limbic Regions in Cntnap2Genes, brain, and behavior · 2026Article
- Analysis of Gene, Environment, and Sex Interaction in the Development of Autistic-like Phenotype in Mice.International journal of molecular sciences · 2026Article
- Multi-region social-emotional network underlying the effects of spine pinching therapy on empathy-like behavior in a rat model of autism spectrum disorder.Frontiers in neuroscience · 2026Article
- Foxp2 mutations and abnormal brain and gastrointestinal development: insights from animal models of speech-language and autism spectrum disorders.Frontiers in neuroanatomy · 2026Review
- The latest research progress of ligustilide in the prevention and treatment of central nervous system disorders.Frontiers in pharmacology · 2026Review
- GABAFrontiers in pharmacology · 2026Review
- Chromatin remodeling factor BAF155 coordinates oligodendroglial-neuronal communications linked to regional myelination and autism-like behavioral deficits in mice.Nature communications · 2025Article
34 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism spectrum disorder (ASD) is thought to result from deviation from normal development of neural circuits and synaptic function. Many genes with mutation in ASD patients have been identified. Here we report that two molecules associated with ASD susceptibility, contactin associated protein-like 2 (CNTNAP2) and Abelson helper integration site-1 (AHI1), are required for synaptic function and ASD-related behavior in mice. Knockdown of CNTNAP2 or AHI1 in layer 2/3 pyramidal neurons of the developing mouse prefrontal cortex (PFC) reduced excitatory synaptic transmission, impaired social interaction and induced mild vocalization abnormality. Although the causes of reduced excitatory transmission were different, pharmacological enhancement of AMPA receptor function effectively restored impaired social behavior in both CNTNAP2- and AHI1-knockdown mice. We conclude that reduced excitatory synaptic transmission in layer 2/3 pyramidal neurons of the PFC leads to impaired social interaction and mild vocalization abnormality in mice.
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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.