ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2019
Psychiatric-disorder-related behavioral phenotypes and cortical hyperactivity in a mouse model of 3q29 deletion syndrome.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 43 citations in OpenAlex.
- Cerebellar mitochondrial dysfunction coincides with structural and behavioral abnormalities in 3q29Del mice.bioRxiv : the preprint server for biology · 2026Article
- Higher frequencies of CNV deletions in bipolar disorder among Chinese Population.Molecular psychiatry · 2026Article
- Article
- Developmentally dynamic, non-convergent transcriptomic profiles in CNV models for schizophrenia risk.Molecular psychiatry · 2026Article
- Driver or passenger? A new assessment of genes in the schizophrenia-associated 3q29 deletion locus for contribution to neurodevelopmental disorders.Journal of neurodevelopmental disorders · 2026Review
- How copy number variations shape brain developmental disorders: Unraveling the synaptic puzzle.Psychiatry and clinical neurosciences · 2026Review
- Risperidone regulates the expression of schizophrenia-related genes in the forebrain of adult male mice.Frontiers in molecular neuroscience · 2026Article
- ESC models of autism with copy-number variations reveal cell-type-specific translational vulnerability.Cell genomics · 2025Article
- Unraveling the enigma of mental disorders: a genetics-first approach and the role of mouse models based on rare disease-susceptible genome variants.Nagoya journal of medical science · 2025Review
- Phenotypes for general behavior, activity, and body temperature in 3q29 deletion model mice.Translational psychiatry · 2024Article
- Search for singularity cells at the onset of brain disorders using whole-brain imaging.Biophysics and physicobiology · 2024Article
- Mechanisms of copy number variants in neuropsychiatric disorders: From genes to therapeutics.Current opinion in neurobiology · 2023Review
- Cross-species analysis identifies mitochondrial dysregulation as a functional consequence of the schizophrenia-associated 3q29 deletion.Science advances · 2023Article
- Shedding light on latent pathogenesis and pathophysiology of mental disorders: The potential of iPS cell technology.Psychiatry and clinical neurosciences · 2023Review
- The molecular pathology of schizophrenia: an overview of existing knowledge and new directions for future research.Molecular psychiatry · 2023Review
- Perceptual pathways to hallucinogenesis.Schizophrenia research · 2022Article
- Molecular brain (micro report) oxytocin ameliorates impaired social behavior in a mouse model of 3q29 deletion syndrome.Molecular brain · 2022Article
- Trends in big data analyses by multicenter collaborative translational research in psychiatry.Psychiatry and clinical neurosciences · 2022Review
- Neuroimaging studies within Cognitive Genetics Collaborative Research Organization aiming to replicate and extend works of ENIGMA.Human brain mapping · 2022Review
- Computational identification of variables in neonatal vocalizations predictive for postpubertal social behaviors in a mouse model of 16p11.2 deletion.Molecular psychiatry · 2021Article
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Authors and funding
21 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
3q29 microdeletion, a rare recurrent copy number variant (CNV), greatly confers an increased risk of psychiatric disorders, such as schizophrenia and autism spectrum disorder (ASD), as well as intellectual disability. However, disease-relevant cellular phenotypes of 3q29 deletion syndrome remain to be identified. To reveal the molecular and cellular etiology of 3q29 deletion syndrome, we generated a mouse model of human 3q29 deletion syndrome by chromosome engineering, which achieved construct validity. 3q29 deletion (Df/+) mice showed reduced body weight and brain volume and, more importantly, impaired social interaction and prepulse inhibition. Importantly, the schizophrenia-related impaired prepulse inhibition was reversed by administration of antipsychotics. These findings are reminiscent of the growth defects and neuropsychiatric behavioral phenotypes in patients with 3q29 deletion syndrome and exemplify that the mouse model achieves some part of face validity and predictive validity. Unbiased whole-brain imaging revealed that neuronal hyperactivation after a behavioral task was strikingly exaggerated in a restricted region of the cortex of Df/+ mice. We further elucidated the cellular phenotypes of neuronal hyperactivation and the reduction of parvalbumin expression in the cortex of Df/+ mice. Thus, the 3q29 mouse model provides invaluable insight into the disease-causative molecular and cellular pathology of psychiatric disorders.
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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.