ArticleBehavioural brain research2013
Autism-related behavioral abnormalities in synapsin knockout mice.
Article in Behavioural brain research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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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.
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Who cites it
74 citing papers in PubMed, 139 citations in OpenAlex.
- Rest-activity patterns across development in two mouse models of autism and epilepsy.Epilepsia open · 2026Article
- Microglia Mitochondria Support Neuronal Maturation via Metabolic and Transcriptional Reprogramming in Human 3D In Vitro Brain Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- NEXMIF overexpression is associated with autism-like behaviors and alterations in dendritic arborization and spine formation in mice.Frontiers in neuroscience · 2025Article
- Memory Decline and Aberration of Synaptic Proteins in X-Linked Moesin Knockout Male Mice.Psychiatry investigation · 2025Article
- Mutation in the mitochondrial chaperone TRAP1 leads to autism with more severe symptoms in males.EMBO molecular medicine · 2024Article
- Molecular profiling of the hippocampus of children with autism spectrum disorder.Molecular psychiatry · 2024Article
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- Molecular and in silico analyses of SYN III gene variants in autism spectrum disorder.Irish journal of medical science · 2023Article
- Low glycemic index diet restrains epileptogenesis in a gender-specific fashion.Cellular and molecular life sciences : CMLS · 2023Article
- Deletion of VPS50 protein in mice brain impairs synaptic function and behavior.bioRxiv : the preprint server for biology · 2023Article
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- Developmental and epileptic encephalopathies: from genetic heterogeneity to phenotypic continuum.Physiological reviews · 2023Review
- Simultaneous Antagonism at H3R/D2R/D3R Reduces Autism-like Self-Grooming and Aggressive Behaviors by Mitigating MAPK Activation in Mice.International journal of molecular sciences · 2022Article
- CRISPR/Cas9-Induced Inactivation of the Autism-Risk GeneInternational journal of molecular sciences · 2022Article
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- Loss of neurodevelopmental-associated miR-592 impairs neurogenesis and causes social interaction deficits.Cell death & disease · 2022Article
- [Mechanism of valproic acid-induced dendritic spine and synaptic impairment in the prefrontal cortex for causing core autistic symptoms in mice].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- The different clinical facets ofFrontiers in cell and developmental biology · 2022Article
14 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
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Several synaptic genes predisposing to autism-spectrum disorder (ASD) have been identified. Nonsense and missense mutations in the SYN1 gene encoding for Synapsin I have been identified in families segregating for idiopathic epilepsy and ASD and genetic mapping analyses have identified variations in the SYN2 gene as significantly contributing to epilepsy predisposition. Synapsins (Syn I/II/III) are a multigene family of synaptic vesicle-associated phosphoproteins playing multiple roles in synaptic development, transmission and plasticity. Lack of SynI and/or SynII triggers a strong epileptic phenotype in mice associated with mild cognitive impairments that are also present in the non-epileptic SynIII(-/-) mice. SynII(-/-) and SynIII(-/-) mice also display schizophrenia-like traits, suggesting that Syns could be involved in the regulation of social behavior. Here, we studied social interaction and novelty, social recognition and social dominance, social transmission of food preference and social memory in groups of male SynI(-/-), SynII(-/-) and SynIII(-/-) mice before and after the appearance of the epileptic phenotype and compared their performances with control mice. We found that deletion of Syn isoforms widely impairs social behaviors and repetitive behaviors, resulting in ASD-related phenotypes. SynI or SynIII deletion altered social behavior, whereas SynII deletion extensively impaired various aspects of social behavior and memory, altered exploration of a novel environment and increased self-grooming. Social impairments of SynI(-/-) and SynII(-/-) mice were evident also before the onset of seizures. The results demonstrate an involvement of Syns in generation of the behavioral traits of ASD and identify Syn knockout mice as a useful experimental model of ASD and epilepsy.
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Registered trials
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.