Myelin modifications after chronic sleep loss in adolescent mice.
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ABSTRACT:
SUBMITTER: Bellesi M
PROVIDER: S-EPMC5946929 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Study objectiveIn humans sleep slow wave activity (SWA) declines during adolescence. It has been suggested that this decline reflects the elimination of cortical synapses, but this hypothesis has never been tested directly.DesignWe focused on mouse frontal cortex and collected data from early adolescence (?postnatal day 20, P20) to adulthood (P60) of (1) SWA; (2) expression of synapsin I, a presynaptic marker; and (3) number of dendritic spines in layers I-II.SettingBasic sleep research laboratory.Patients or participantsYFP-line H mice (n = 70; P15-87, all males) and GFP-line S mice (n = 14; P17-60, 8 females) were used for EEG recording. Forty-five YFP mice (P19-119, 12 females) and 42 GFP-S mice (P20-60, 14 females) were used for in vivo 2-photon imaging and ex vivo confocal microscopy, respectively. Other YGP mice (n = 57, P10-77) were used for western blot analysis of synapsin I.InterventionsN/A.Measurements and resultsAs in humans, SWA in mice declined from early adolescence to adulthood. Synapsin I levels increased from P10 to P24, with little change afterwards. Mean spine density in apical dendrites of layer V pyramidal neurons (YFP-H) showed no change from P20 to P60. Spine number in layers I-II apical dendrites, belonging to layer III and V pyramidal neurons (GFP-S), increased slightly from P20 to P30 and decreased from P30 to P60; smaller spines decreased in number from P20 to P60, while bigger spines increased.ConclusionsIn mice, it is unlikely that the developmental decrease in SWA can be accounted for by a net pruning of cortical synapses.
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