ArticleAutism research : official journal of the International Society for Autism Research2017
Hyperactivity and male-specific sleep deficits in the 16p11.2 deletion mouse model of autism.
Article in Autism research : official journal of the International Society for Autism Research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 90 citations in OpenAlex.
- Review
- Complement contributes to hyperactive behavior in the 16p11.2 hemideletion mouse model.Brain, behavior, and immunity · 2026Article
- Sex-specific role of body weight in mediating stress susceptibility through MeA Tac2-Nk3R signaling.Translational psychiatry · 2026Article
- 16p11.2 duplication and NMDA receptor antagonism have distinct impacts on reward learning and decision making.Psychopharmacology · 2026Article
- Postnatal reduction of eIF4E overexpression in D1-SPNs ameliorates KCNQ channel dysfunction, hyperexcitability and ASD-like behaviours.Cellular and molecular life sciences : CMLS · 2026Article
- A chromosome region linked to neurodevelopmental disorders influences locomotor behavior through sex-specific neural circuits.Nature communications · 2026Article
- Sex-dependent prediction of autism.Frontiers in genetics · 2026Article
- Placental Igf1 overexpression sex-specifically impacts mouse placenta structure, altering offspring striatal development and behavior.Experimental neurology · 2025Article
- 16p11.2 duplication shows early male-biased impacts on reward learning, but NMDA receptor antagonism reduces optimal choice selection in both wildtypes and 16p11.2 duplication.bioRxiv : the preprint server for biology · 2025Article
- Article
- Circadian activity and sleep architecture in autism spectrum disorder mouse model withFrontiers in sleep · 2025Article
- Circuit mechanism underlying fragmented sleep and memory deficits in 16p11.2 deletion mouse model of autism.iScience · 2024Article
- The pleiotropic spectrum of proximal 16p11.2 CNVs.American journal of human genetics · 2024Review
- Circuit mechanism underlying fragmented sleep and memory deficits in 16p11.2 deletion mouse model of autism.bioRxiv : the preprint server for biology · 2024Article
- Dissecting 16p11.2 hemi-deletion to study sex-specific striatal phenotypes of neurodevelopmental disorders.Molecular psychiatry · 2024Article
- Circuit mechanism underlying fragmented sleep and memory deficits in 16p11.2 deletion mouse model of autism.Research square · 2024Article
- Orthologs ofSleep advances : a journal of the Sleep Research Society · 2024Article
- Understanding copy number variations through their genes: a molecular view on 16p11.2 deletion and duplication syndromes.Frontiers in pharmacology · 2024Review
- A cluster of neuropeptide S neurons regulates breathing and arousal.Current biology : CB · 2023Article
- Targeting NR1D1 in organ injury: challenges and prospects.Military Medical Research · 2023Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Sleep disturbances and hyperactivity are prevalent in several neurodevelopmental disorders, including autism spectrum disorders (ASDs) and attention deficit-hyperactivity disorder (ADHD). Evidence from genome-wide association studies indicates that chromosomal copy number variations (CNVs) are associated with increased prevalence of these neurodevelopmental disorders. In particular, CNVs in chromosomal region 16p11.2 profoundly increase the risk for ASD and ADHD, disorders that are more common in males than females. We hypothesized that mice hemizygous for the 16p11.2 deletion (16p11.2 del/+) would exhibit sex-specific sleep and activity alterations. To test this hypothesis, we recorded activity patterns using infrared beam breaks in the home-cage of adult male and female 16p11.2 del/+ and wildtype (WT) littermates. In comparison to controls, we found that both male and female 16p11.2 del/+ mice exhibited robust home-cage hyperactivity. In additional experiments, sleep was assessed by polysomnography over a 24-hr period. 16p11.2 del/+ male, but not female mice, exhibited significantly more time awake and significantly less time in non-rapid-eye-movement (NREM) sleep during the 24-hr period than wildtype littermates. Analysis of bouts of sleep and wakefulness revealed that 16p11.2 del/+ males, but not females, spent a significantly greater proportion of wake time in long bouts of consolidated wakefulness (greater than 42 min in duration) compared to controls. These changes in hyperactivity, wake time, and wake time distribution in the males resemble sleep disturbances observed in human ASD and ADHD patients, suggesting that the 16p11.2 del/+ mouse model may be a useful genetic model for studying sleep and activity problems in human neurodevelopmental disorders. Autism Res 2016. © 2016 International Society for Autism Research, Wiley Periodicals, Inc. Autism Res 2017, 10: 572-584. © 2016 International Society for Autism Research, Wiley Periodicals, Inc.
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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 Socratic graph.