Sleep Patterns and Homeostatic Mechanisms in Adolescent Mice

Sleep changes were studied in mice (n = 59) from early adolescence to adulthood (postnatal days P19–111). REM sleep declined steeply in early adolescence, while total sleep remained constant and NREM sleep increased slightly. Four hours of sleep deprivation starting at light onset were performed fro...

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Main Authors: Giulio Tononi, Jeffrey T. Zoltan, Ugo Faraguna, Aaron B. Nelson, Chiara Cirelli
Format: Article
Language:English
Published: MDPI AG 2013-03-01
Series:Brain Sciences
Subjects:
Online Access:http://www.mdpi.com/2076-3425/3/1/318
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spelling doaj-7cbb64c500334beeafd0d37e12afaac62020-11-24T22:21:25ZengMDPI AGBrain Sciences2076-34252013-03-013131834310.3390/brainsci3010318Sleep Patterns and Homeostatic Mechanisms in Adolescent MiceGiulio TononiJeffrey T. ZoltanUgo FaragunaAaron B. NelsonChiara CirelliSleep changes were studied in mice (n = 59) from early adolescence to adulthood (postnatal days P19–111). REM sleep declined steeply in early adolescence, while total sleep remained constant and NREM sleep increased slightly. Four hours of sleep deprivation starting at light onset were performed from ages P26 through adulthood (>P60). Following this acute sleep deprivation all mice slept longer and with more consolidated sleep bouts, while NREM slow wave activity (SWA) showed high interindividual variability in the younger groups, and increased consistently only after P42. Three parameters together explained up to 67% of the variance in SWA rebound in frontal cortex, including weight-adjusted age and increase in alpha power during sleep deprivation, both of which positively correlated with the SWA response. The third, and strongest predictor was the SWA decline during the light phase in baseline: mice with high peak SWA at light onset, resulting in a large SWA decline, were more likely to show no SWA rebound after sleep deprivation, a result that was also confirmed in parietal cortex. During baseline, however, SWA showed the same homeostatic changes in adolescents and adults, declining in the course of sleep and increasing across periods of spontaneous wake. Thus, we hypothesize that, in young adolescent mice, a ceiling effect and not the immaturity of the cellular mechanisms underlying sleep homeostasis may prevent the SWA rebound when wake is extended beyond its physiological duration.http://www.mdpi.com/2076-3425/3/1/318adolescencecerebral cortexsleep deprivationslow wave activity
collection DOAJ
language English
format Article
sources DOAJ
author Giulio Tononi
Jeffrey T. Zoltan
Ugo Faraguna
Aaron B. Nelson
Chiara Cirelli
spellingShingle Giulio Tononi
Jeffrey T. Zoltan
Ugo Faraguna
Aaron B. Nelson
Chiara Cirelli
Sleep Patterns and Homeostatic Mechanisms in Adolescent Mice
Brain Sciences
adolescence
cerebral cortex
sleep deprivation
slow wave activity
author_facet Giulio Tononi
Jeffrey T. Zoltan
Ugo Faraguna
Aaron B. Nelson
Chiara Cirelli
author_sort Giulio Tononi
title Sleep Patterns and Homeostatic Mechanisms in Adolescent Mice
title_short Sleep Patterns and Homeostatic Mechanisms in Adolescent Mice
title_full Sleep Patterns and Homeostatic Mechanisms in Adolescent Mice
title_fullStr Sleep Patterns and Homeostatic Mechanisms in Adolescent Mice
title_full_unstemmed Sleep Patterns and Homeostatic Mechanisms in Adolescent Mice
title_sort sleep patterns and homeostatic mechanisms in adolescent mice
publisher MDPI AG
series Brain Sciences
issn 2076-3425
publishDate 2013-03-01
description Sleep changes were studied in mice (n = 59) from early adolescence to adulthood (postnatal days P19–111). REM sleep declined steeply in early adolescence, while total sleep remained constant and NREM sleep increased slightly. Four hours of sleep deprivation starting at light onset were performed from ages P26 through adulthood (>P60). Following this acute sleep deprivation all mice slept longer and with more consolidated sleep bouts, while NREM slow wave activity (SWA) showed high interindividual variability in the younger groups, and increased consistently only after P42. Three parameters together explained up to 67% of the variance in SWA rebound in frontal cortex, including weight-adjusted age and increase in alpha power during sleep deprivation, both of which positively correlated with the SWA response. The third, and strongest predictor was the SWA decline during the light phase in baseline: mice with high peak SWA at light onset, resulting in a large SWA decline, were more likely to show no SWA rebound after sleep deprivation, a result that was also confirmed in parietal cortex. During baseline, however, SWA showed the same homeostatic changes in adolescents and adults, declining in the course of sleep and increasing across periods of spontaneous wake. Thus, we hypothesize that, in young adolescent mice, a ceiling effect and not the immaturity of the cellular mechanisms underlying sleep homeostasis may prevent the SWA rebound when wake is extended beyond its physiological duration.
topic adolescence
cerebral cortex
sleep deprivation
slow wave activity
url http://www.mdpi.com/2076-3425/3/1/318
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