title: Sleep-wake architecture in mouse models for Down syndrome.
abstract: Sleep-wake homeostasis is crucial for behavioral performances and memory both in the general population and in patients with learning disability, among whom were Down syndrome (DS) patients. We investigated, in mouse models of DS, cortical EEG and sleep-wake architecture under baseline conditions and after a 4-h sleep deprivation (SD). Young hemizygous mice (hSODwt/+) transgenic for the human CuZn superoxide dismutase (hSOD1) or for the human amyloid precursor protein (HuAPP(695); hAPPwt/+) were obtained on the same FVB/N inbred background. Baseline records for slow wave sleep (SWS) and wake (W) parameters were unchanged, whereas paradoxical sleep (PS) episode numbers were decreased and PS latency increased after lights off in hSODwt/+ mice versus controls. hSODwt/+ mice did not experience SWS or PS rebounds after SD but EEG activity in the delta-SWS activity (SWA) was enhanced. hAPPwt/+ mice exhibited no change in PS but an increase in W and a decrease in SWS before light transition as well as an increase in theta-power in PS and W. After SD, hAPPwt/+ mice exhibited SWS and PS rebounds as well as enhancement of SWA. We investigated also the nitrite/nitrate levels in all mice and found an increase in the brainstem of hSODwt/+ mice only versus control ones. These preliminary data provide useful results to investigate other genetically manipulated mice and to better understand the biochemical basis of sleep disorders in DS patients.
authors.affiliation: Unite INSERM Unit 480, Claude Bernard University, 69373 Lyon Cedex 08, France.
authors.forename: Damien
authors.initials: D
authors.lastname: Colas
authors.forename: Jacqueline
authors.initials: J
authors.lastname: London
authors.forename: Abdallah
authors.initials: A
authors.lastname: Gharib
authors.forename: Raymond
authors.initials: R
authors.lastname: Cespuglio
authors.forename: Nicole
authors.initials: N
authors.lastname: Sarda
mesh_terms: D000818:Animals; D001933:Brain Stem / Q000378:metabolism / Q000503:physiopathology; D002540:Cerebral Cortex / Q000378:metabolism / Q000503:physiopathology; D004195:Disease Models, Animal; D004314:Down Syndrome / Q000378:metabolism* / Q000503:physiopathology*; D051379:Mice; D008822:Mice, Transgenic; D009566:Nitrates / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D009573:Nitrites / Q000378:metabolism; D012890:Sleep / Q000502:physiology; D020178:Sleep Disorders, Circadian Rhythm / Q000378:metabolism* / Q000503:physiopathology*; D013482:Superoxide Dismutase / Q000235:genetics*; D000072105:Superoxide Dismutase-1; D014851:Wakefulness / Q000502:physiology
chemical_list: D009566:Nitrates; D009573:Nitrites; C000606290:SOD1 protein, human; D009569:Nitric Oxide; C000606291:Sod1 protein, mouse; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1