ArticlePloS one2010
Decreased exploratory activity in a mouse model of 15q duplication syndrome; implications for disturbance of serotonin signaling.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 118 citations in OpenAlex.
- Dup15q model mice exhibit impaired gastrointestinal motility and a constipation-like phenotype, alleviated by prucalopride.Translational psychiatry · 2026Article
- The role of NLRP3 neuroinflammation in cognitive frailty diversity during aging and after LPS administration in mice.Scientific reports · 2026Article
- RO4938581, a GABAMolecular psychiatry · 2026Article
- Duplication of the autism-related gene Chd8 leads to behavioral hyperactivity and neurodevelopmental defects in mice.Nature communications · 2025Article
- Autism spectrum disorder-like behaviors induced by hyper-glutamatergic NMDA receptor signaling through hypo-serotonergic 5-HTNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Social circuits and their dysfunction in autism spectrum disorder.Molecular psychiatry · 2023Review
- Galnt17 loss-of-function leads to developmental delay and abnormal coordination, activity, and social interactions with cerebellar vermis pathology.Developmental biology · 2022Article
- The prevention of home-cage grid climbing affects muscle strength in mice.Scientific reports · 2022Article
- No evidence of spatial representation of age, but "own-age bias" like face processing found in chimpanzees.Animal cognition · 2022Article
- Translational Magnetic Resonance Imaging in Autism Spectrum Disorder From the Mouse Model to Human.Frontiers in neuroscience · 2022Review
- Genetic dissection identifies Necdin as a driver gene in a mouse model of paternal 15q duplications.Nature communications · 2021Article
- Mice with mutations in Trpm1, a gene in the locus of 15q13.3 microdeletion syndrome, display pronounced hyperactivity and decreased anxiety-like behavior.Molecular brain · 2021Article
- Implications of germline copy-number variations in psychiatric disorders: review of large-scale genetic studies.Journal of human genetics · 2021Review
- An Unbiased Drug Screen for Seizure Suppressors in Duplication 15q Syndrome Reveals 5-HTBiological psychiatry · 2020Article
- Upregulated 5-HTMolecular brain · 2020Article
- A social encounter drives gene expression changes linked to neuronal function, brain development, and related disorders in mice expressing the serotonin transporter Ala56 variant.Neuroscience letters · 2020Article
- Effects of repetitive gentle handling of male C57BL/6NCrl mice on comparative behavioural test results.Scientific reports · 2020Article
- Awake functional MRI detects neural circuit dysfunction in a mouse model of autism.Science advances · 2020Article
- Behavioral analysis in mice deficient for GAREM2 (Grb2-associated regulator of Erk/MAPK subtype2) that is a subtype of highly expressing in the brain.Molecular brain · 2019Article
- Recent genetic and functional insights in autism spectrum disorder.Current opinion in neurology · 2019Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism spectrum disorders (ASDs) have garnered significant attention as an important grouping of developmental brain disorders. Recent genomic studies have revealed that inherited or de novo copy number variations (CNVs) are significantly involved in the pathophysiology of ASDs. In a previous report from our laboratory, we generated mice with CNVs as a model of ASDs, with a duplicated mouse chromosome 7C that is orthologous to human chromosome 15q11-13. Behavioral analyses revealed paternally duplicated (patDp/+) mice displayed abnormal behaviors resembling the symptoms of ASDs. In the present study, we extended these findings by performing various behavioral tests with C57BL/6J patDp/+ mice, and comprehensively measuring brain monoamine levels with ex vivo high performance liquid chromatography. Compared with wild-type controls, patDp/+ mice exhibited decreased locomotor and exploratory activities in the open field test, Y-maze test, and fear-conditioning test. Furthermore, their decreased activity levels overcame increased appetite induced by 24 hours of food deprivation in the novelty suppressed feeding test. Serotonin levels in several brain regions of adult patDp/+ mice were lower than those of wild-type control, with no concurrent changes in brain levels of dopamine or norepinephrine. Moreover, analysis of monoamines in postnatal developmental stages demonstrated reduced brain levels of serotonin in young patDp/+ mice. These findings suggest that a disrupted brain serotonergic system, especially during postnatal development, may generate the phenotypes of patDp/+ mice.
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