ArticleJournal of neurodevelopmental disorders2016
Limited impact of Cntn4 mutation on autism-related traits in developing and adult C57BL/6J mice.
Article in Journal of neurodevelopmental disorders, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Auditory processing in rodent models of autism: a systematic review.Journal of neurodevelopmental disorders · 2022Pooled it
- Cntn4 Gene Deficiency Promotes Autism-Like Phenotypes Associated with Gut Microbiota Perturbations and Gut-Brain Axis Metabolomic Alterations in Mice.Molecular neurobiology · 2025Article
- Molecular mechanism of contactin 2 homophilic interaction.Structure (London, England : 1993) · 2024Article
- CNTN4 modulates neural elongation through interplay with APP.Open biology · 2024Article
- Morphometric Integrated Classification Index: A Multisite Model-Based, Interpretable, Shareable and Evolvable Biomarker for Schizophrenia.Schizophrenia bulletin · 2022Article
- Detection of copy number variation associated with ventriculomegaly in fetuses using single nucleotide polymorphism arrays.Scientific reports · 2021Article
- Cntn4, a risk gene for neuropsychiatric disorders, modulates hippocampal synaptic plasticity and behavior.Translational psychiatry · 2021Article
- Cell Adhesion Molecules Involved in Neurodevelopmental Pathways Implicated in 3p-Deletion Syndrome and Autism Spectrum Disorder.Frontiers in cellular neuroscience · 2020Review
- Structural abnormalities in the primary somatosensory cortex and a normal behavioral profile in Contactin-5 deficient mice.Cell adhesion & migration · 2018Article
- Heterogeneity of Cell Surface Glutamate and GABA Receptor Expression in Shank and CNTN4 Autism Mouse Models.Frontiers in molecular neuroscience · 2018Article
- IntragenicMolecular syndromology · 2017Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMouse models offer an essential tool to unravel the impact of genetic mutations on autism-related phenotypes. The behavioral impact of some important candidate gene models for autism spectrum disorder (ASD) has not yet been studied, and existing characterizations mostly describe behavioral phenotypes at adult ages, disregarding the developmental nature of the disorder. In this context, the behavioral influence of CNTN4, one of the strongest suggested ASD candidate genes, is unknown. Here, we used our recently established developmental test battery to characterize the consequences of disruption of contactin 4 (Cntn4) on neurological, sensory, cognitive, and behavioral phenotypes across different developmental stages.
methodsC57BL/6J mice with heterozygous and homozygous disruption of Cntn4 were studied through an extensive, partially longitudinal, test battery at various developmental stages, including various paradigms testing social and restricted repetitive behaviors.
resultsDevelopmental neurological and cognitive screenings revealed no significant differences between genotypes, and ASD-related behavioral domains were also unchanged in Cntn4-deficient versus wild-type mice. The impact of Cntn4-deficiency was found to be limited to increased startle responsiveness following auditory stimuli of different high amplitudes in heterozygous and homozygous Cntn4-deficient mice and enhanced acquisition in a spatial learning task in homozygous mice.
conclusionsDisruption of Cntn4 in the C57BL/6J background does not affect specific autism-related phenotypes in developing or adult mice but causes subtle non-disorder specific changes in sensory behavioral responses and cognitive performance.
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