Polysomnography in transgenic hSOD1 mice as Down syndrome model.
Sleep-wake homeostasis is crucial for behavioral performances and memory in the general population and in learning disability populations among them Down syndrome patients. We investigated, in a mouse model of Down syndrome, cortical EEG and sleep-wake architecture under baseline conditions and after a 4 hr sleep deprivation (SD). Young heterozygous transgenic mice (S/+) for the human Cu/Zn superoxide dismutase (hSOD-1) were obtained on FVB/N background. Baseline records for slow wave sleep (SWS) and wake (W) parameters were the same in S/+ and control mice whereas paradoxical sleep (PS) episode number decreased and PS latency increased after light off in S/+ mice. These data correlate well the polysomnographic phenotype of young DS patients.
Colas
D
D
INSERM Unit 480, Claude Bernard University, Lyon, France.
London
J
J
Cespuglio
R
R
Sarda
N
N
D000818:Animals; D004195:Disease Models, Animal; D004314:Down Syndrome / Q000201:enzymology* / Q000235:genetics; D006801:Humans; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D017286:Polysomnography / Q000379:methods*; D012894:Sleep Stages / Q000235:genetics / Q000502:physiology*; D013482:Superoxide Dismutase / Q000096:biosynthesis* / Q000235:genetics; D000072105:Superoxide Dismutase-1
C000606290:SOD1 protein, human; C000606291:Sod1 protein, mouse; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1