ArticleScientific reports2017
The natural Disc1-deletion present in several inbred mouse strains does not affect sleep.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 15 citations in OpenAlex.
- Adolescent sleep defects and dopaminergic hyperactivity in mice with a schizophrenia-linked Shank3 mutation.Sleep · 2023Article
- Distinct translatome changes in specific neural populations precede electroencephalographic changes in prion-infected mice.PLoS pathogens · 2022Article
- Article
- Slc1a3-2A-CreERT2 mice reveal unique features of Bergmann glia and augment a growing collection of Cre drivers and effectors in the 129S4 genetic background.Scientific reports · 2021Article
- Disrupted-in-schizophrenia 1 enhances the quality of circadian rhythm by stabilizing BMAL1.Translational psychiatry · 2021Article
- Sleep Disorders in Children With Autism Spectrum Disorder: Insights From Animal Models, Especially Non-human Primate Model.Frontiers in behavioral neuroscience · 2021Review
- Sleep-Wake Rhythm and Oscillatory Pattern Analysis in a Multiple Hit Schizophrenia Rat Model (Wisket).Frontiers in behavioral neuroscience · 2021Article
- Phenotypic characteristics of commonly used inbred mouse strains.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Sleep, brain development, and autism spectrum disorders: Insights from animal models.Journal of neuroscience research · 2020Review
- Article
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3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The gene Disrupted in Schizophrenia-1 (DISC1) is linked to a range of psychiatric disorders. Two recent transgenic studies suggest DISC1 is also involved in homeostatic sleep regulation. Several strains of inbred mice commonly used for genome manipulation experiments, including several Swiss and likely all 129 substrains, carry a natural deletion mutation of Disc1. This constitutes a potential confound for studying sleep in genetically modified mice. Since disturbed sleep can also influence psychiatric and neurodegenerative disease models, this putative confound might affect a wide range of studies in several fields. Therefore, we asked to what extent the natural Disc1 deletion affects sleep. To this end, we first compared sleep and electroencephalogram (EEG) phenotypes of 129S4 mice carrying the Disc1 deletion and C57BL/6N mice carrying the full-length version. We then bred Disc1 from C57BL/6N into the 129S4 background, resulting in S4-Disc1 mice. The differences between 129S4 and C57BL/6N were not detected in the 129S4 to S4-Disc1 comparison. We conclude that the mutation has no effect on the measured sleep and EEG characteristics. Thus, it is unlikely the widespread Disc1 deletion has led to spurious results in previous sleep studies or that it alters sleep in mouse models of psychiatric or neurodegenerative diseases.
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