ArticleBehavioural brain research2019
Juvenile Shank3b deficient mice present with behavioral phenotype relevant to autism spectrum disorder.
Article in Behavioural brain research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Developmental CA2 perineuronal net reduction restores social memory in Shank3 mutant mice.Communications biology · 2026Article
- Developmental CA2 perineuronal net reduction restores social memory inbioRxiv : the preprint server for biology · 2025Article
- Article
- Autism-like phenotype across the lifespan of Shank3B-mutant mice of both sexes.Journal of neurodevelopmental disorders · 2025Article
- Diminished Motivation for Voluntary Exercise and Metabolic Dysfunction in Psychiatric Disorders: A Behavioral Perspective on Autism Spectrum Disorder and Depression.International neurourology journal · 2025Article
- Missense mutation in the activation segment of the kinase CK2 models Okur-Chung neurodevelopmental disorder and alters the hippocampal glutamatergic synapse.Molecular psychiatry · 2025Article
- Gut microbiota diversity is altered in a sex-dependent manner in Shank3B heterozygote mice.Frontiers in microbiomes · 2025Article
- Hyperthermia elevates brain temperature and improves behavioural signs in animal models of autism spectrum disorder.Molecular autism · 2023Article
- Targeting Shank3 deficiency and paresthesia in autism spectrum disorder: A brief review.Frontiers in molecular neuroscience · 2023Review
- Association of SHANK Family with Neuropsychiatric Disorders: An Update on Genetic and Animal Model Discoveries.Cellular and molecular neurobiology · 2022Review
- Sex-Dependent Social and Repetitive Behavior and Neurochemical Profile in Mouse Model of Autism Spectrum Disorder.Metabolites · 2022Article
- Integration of structural MRI and epigenetic analyses hint at linked cellular defects of the subventricular zone and insular cortex in autism: Findings from a case study.Frontiers in neuroscience · 2022Article
- Ultrasonic vocalizations in mice: relevance for ethologic and neurodevelopmental disorders studies.Neural regeneration research · 2021Review
- LMT USV Toolbox, a Novel Methodological Approach to Place Mouse Ultrasonic Vocalizations in Their Behavioral Contexts-A Study in Female and Male C57BL/6J Mice and inFrontiers in behavioral neuroscience · 2021Article
- A DLG2 deficiency in mice leads to reduced sociability and increased repetitive behavior accompanied by aberrant synaptic transmission in the dorsal striatum.Molecular autism · 2020Article
- Enhanced Glutamatergic Currents at Birth in Shank3 KO Mice.Neural plasticity · 2019Article
- Article
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Authors and funding
9 authors.
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Abstract
Autism spectrum disorder (ASD) is a pervasive, multifactorial neurodevelopmental disorder diagnosed according to deficits in three behavioral domains: communication, social interaction, and stereotyped/repetitive behaviors. Mutations in Shank genes account for ∼1% of clinical ASD cases with Shank3 being the most common gene variant. In addition to maintaining synapses and facilitating dendritic maturation, Shank genes encode master scaffolding proteins that build core complexes in the postsynaptic densities of glutamatergic synapses. Male mice with a deletion of the PDZ domain of Shank3 (Shank3B KO) were previously shown to display ASD-like behavioral phenotypes with reported self-injurious repetitive grooming and aberrant social interactions. Our goal was to extend these previous findings and use a comprehensive battery of highly detailed ASD-relevant behavioral assays including an assessment of mouse ultrasonic communication carried out on key developmental days and male and female Shank3B KO mice. We demonstrate that ASD-related behaviors, atypical reciprocal social interaction and indiscriminate repetitive grooming, are apparent in juvenile stages of development of Shank3B KO mice. Our findings underscore the importance of utilizing Shank mutant models to understand the impact of this gene in ASD etiology, whichmay enable future studies focusing on etiological gene-environment interactions in ASD.
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