Abstract

Approximately one-third of adolescents and adults in developed countries regularly experience insufficient sleep across the school and/or work week interspersed with weekend catch up sleep. This common practice of weekend recovery sleep reduces subjective sleepiness, yet recent studies demonstrate that one weekend of recovery sleep may not be sufficient in all persons to fully reverse all neurobehavioral impairments observed with chronic sleep loss, particularly vigilance. Moreover, recent studies in animal models demonstrate persistent injury to and loss of specific neuron types in response to chronic short sleep (CSS) with lasting effects on sleep/wake patterns. Here, we provide a comprehensive review of the effects of chronic sleep disruption on neurobehavioral performance and injury to neurons, astrocytes, microglia, and oligodendrocytes and discuss what is known and what is not yet established for reversibility of neural injury. Recent neurobehavioral findings in humans are integrated with animal model research examining long-term consequences of sleep loss on neurobehavioral performance, brain development, neurogenesis, neurodegeneration, and connectivity. While it is now clear that recovery of vigilance following short sleep requires longer than one weekend, less is known of the impact of CSS on cognitive function, mood, and brain health long term. From work performed in animal models, CSS in the young adult and short-term sleep loss in critical developmental windows can have lasting detrimental effects on neurobehavioral performance.

Highlights

  • One-third of adolescents and adults in developed countries regularly experience insufficient sleep across the school and/or work week interspersed with weekend catch up sleep

  • If animals exposed to this severe sleep loss do not incur obvious neurodegeneration, should we expect injury with the less severe chronic sleep restriction, as experienced by humans? Several important considerations are necessary to most accurately address this question

  • Sleep-deprived animals in this platform paradigm were compared to yoked control animals that were exposed to single housing on a platform over water where some sleep loss and sleep fragmentation occurred in these yoked controls

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Summary

PROTRACTED RECOVERY OF NEUROBEHAVIORAL IMPAIRMENT FOLLOWING CSS IN HUMANS

Contrary to the widely appreciated subjective normalization of sleepiness after a weekend of recovery sleep, several studies have shown clearly that shortened sleep across 1 week in healthy adults produces cumulative impairments in vigilance with incomplete recovery after three full nights of recovery sleep [2, 18, 19]. When adolescents are restricted to 4 h sleep per night for seven nights, processing speed remained slowed even after two full recovery nights of sleep [23] These findings support: [1] recovery requiring >3 nights for specific neurobehavioral performances; [2] a differential susceptibility to CSS across various tasks, where vigilance is sensitive to CSS; [3] a differential susceptibility for age in that adolescents may require longer to recover from CSS neurobehavioral impairments; and [4] recovery of circuits integral to behavioral state and/or vigilance is delayed following CSS

ANIMAL MODELS OF SLEEP LOSS
NEURAL FINDINGS IN THE RECHTSCHAFFEN RAT STUDIES OF SLEEP DEPRIVATION
Adult mice
Locus Coeruleus Response to Unihemispheric Sleep
CHRONIC SLEEP RESTRICTION EFFECTS ON VIGILANCE IN ANIMAL MODELS
SIMILARITIES AND DIFFERENCES WITH EFFECTS OF SLEEP FRAGMENTATION VS CSS
SLEEP LOSS
NEURAL CONSEQUENCES OF SLEEP LOSS DURING BRAIN DEVELOPMENT
EFFECTS OF SLEEP LOSS ON NEUROGENESIS
EFFECTS OF SLEEP LOSS ON
EFFECTS OF SLEEP LOSS ON HIPPOCAMPAL FUNCTION AND CONNECTIVITY
CONCLUDING REMARKS
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