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dc.contributor.authorBaud, Maxime O.
dc.contributor.authorMagistretti, Pierre J.
dc.contributor.authorPetit, Jean Marie
dc.date.accessioned2015-08-03T12:33:39Z
dc.date.available2015-08-03T12:33:39Z
dc.date.issued2015-04-01
dc.identifier.issn01618105
dc.identifier.pmid25325477
dc.identifier.doi10.5665/sleep.4572
dc.identifier.urihttp://hdl.handle.net/10754/564135
dc.description.abstractStudy Objectives: Sleep fragmentation (SF) is an integral feature of sleep apnea and other prevalent sleep disorders. Although the effect of repetitive arousals on cognitive performance is well documented, the effects of long-term SF on electroencephalography (EEG) and molecular markers of sleep homeostasis remain poorly investigated. To address this question, we developed a mouse model of chronic SF and characterized its effect on EEG spectral frequencies and the expression of genes previously linked to sleep homeostasis including clock genes, heat shock proteins, and plasticity-related genes. Design: N/A. Setting: Animal sleep research laboratory. Participants : Sixty-six C57BL6/J adult mice. Interventions: Instrumental sleep disruption at a rate of 60/h during 14 days Measurements and Results: Locomotor activity and EEG were recorded during 14 days of SF followed by recovery for 2 days. Despite a dramatic number of arousals and decreased sleep bout duration, SF minimally reduced total quantity of sleep and did not significantly alter its circadian distribution. Spectral analysis during SF revealed a homeostatic drive for slow wave activity (SWA; 1-4 Hz) and other frequencies as well (4-40 Hz). Recordings during recovery revealed slow wave sleep consolidation and a transient rebound in SWA, and paradoxical sleep duration. The expression of selected genes was not induced following chronic SF. Conclusions: Chronic sleep fragmentation (SF) increased sleep pressure confirming that altered quality with preserved quantity triggers core sleep homeostasis mechanisms. However, it did not induce the expression of genes induced by sleep loss, suggesting that these molecular pathways are not sustainably activated in chronic diseases involving SF.
dc.description.sponsorshipThis work was supported by a Swiss National Science Foundation grant (3100AO-108336/1) to Dr. Magistretti. Dr. Baud's work was directly supported by a Swiss National Science Foundation personal MD-PhD grant (323600-119351/1). The authors have indicated no financial conflicts of interest.
dc.publisherAssociated Professional Sleep Societies (APSS)
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4355896
dc.subjectBDNF
dc.subjectHeat shock proteins
dc.subjectParadoxical sleep
dc.subjectSleep apneas
dc.subjectSleep fragmentation
dc.subjectSlow waves
dc.subjectSpindles
dc.subjectSWA
dc.titleSustained sleep fragmentation induces sleep homeostasis in mice
dc.typeArticle
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Division
dc.contributor.departmentBioscience Program
dc.identifier.journalSLEEP
dc.identifier.pmcidPMC4355896
dc.contributor.institutionLaboratory of Neuroenergetic and Cellular Dynamics, Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL)Lausanne, Switzerland
dc.contributor.institutionDepartment of Neurology, University of California at San Francisco (UCSF), 505 Parnassus AvenueSan Francisco, CA, United States
dc.contributor.institutionCentre de Neurosciences Psychiatriques, Department of Psychiatry, Centre Hospitalier Universitaire VaudoisPrilly, Switzerland
kaust.personMagistretti, Pierre J.


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