Loss of Sleep Affects the Ultrastructure of Pyramidal Neurons in the Adolescent Mouse Frontal Cortex

Vivo, Luisa de; Nelson, Aaron; Bellesi, Michele; Noguti, Juliana; Tononi, Giulio; Cirelli, Chiara

doi:10.5665/sleep.5644

Cited by 38 publications

(42 citation statements)

References 63 publications

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“…Based on a 12:12 dark/light cycle, the animals were sleep deprived starting 4 hours after lights came on for 4 hours. Sleep deprivation was achieved through continual low stress sleep disturbances including cage tapping and gentle stroking of the back with a small brush [14][15]. Mice were subjected to 4 consecutive days of sleep deprivation 4 hours each day, followed by immediate behavior testing after the last sleepdeprivation session.…”

Section: Sleep Deprivation Proceduresmentioning

confidence: 99%

Sleep-deprived cognitive impairment in aging mice is alleviated by rapamycin

Mukherjee

Lee

Zhu

et al. 2019

APT

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Objective: Sleep deprivation-induced cognitive impairment is a major health concern and an age-related risk factor for dementia. There is an urgent need to develop ways of preventing the adverse neurological effects of sleep deprivation, but current preclinical animal models of short-term sleep deprivation are not well described. Methods: C57BL6 mice of varying ages were sleep deprived for 4 hours a day for 4 days, and then tested with a Box maze navigation task. Results: Sleep deprived mice at young, middle and older ages showed learning impairment that varied by strain and gender. In general, females were more sensitive to sleep deprivation than males. To determine whether sleep deprivation-induced learning impairment would respond to therapeutic intervention, an independent cohort of mice was treated with rapamycin daily during the 4 days of sleep deprivation. Mice that were sleep deprived and treated with rapamycin showed significant improvement in learning time suggesting that the cognitive impairment might be associated in part with molecular and cellular mechanisms targeted by rapamycin. Conclusions: The observations from this study suggest that aging mice would be productive models to study pathobiology and therapeutic intervention of cognitive impairment triggered by age-related sleeping disorders in people.

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Section: Sleep Deprivation Proceduresmentioning

confidence: 99%

Sleep-deprived cognitive impairment in aging mice is alleviated by rapamycin

Mukherjee

Lee

Zhu

et al. 2019

APT

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“…Spontaneous, induced, and/or enriched waking experience can increase synapse number, size, and/ or synaptic protein levels in multiple brain regions, which can be reversed by sleep (Donlea et al 2009;Gilestro et al 2009;Hanlon et al 2009;Bushey et al 2011;de Vivo et al 2016de Vivo et al , 2017. Which of these synaptic changes mediate homeostatic sleep drive?…”

Section: Glutamatementioning

confidence: 99%

Molecular Mechanisms of Sleep Homeostasis in Flies and Mammals

Allada¹,

Cirelli

Sehgal

2017

Cold Spring Harb Perspect Biol

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133

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“…At the cellular level, there are several reasons why the wake-related increase in synaptic strength is costly. One reason is the high energy consumption required to sustain synaptic activity5, which is expected to increase with increasing synaptic strength in wake, resulting in higher mitochondrial activity during sustained wake relative to sleep6789. In the cerebral cortex, oxidants production linked to mitochondrial activity increases during extended wake with exploration10, and wake-related metabolic activation puts locus coeruleus noradrenergic cells, and other wake-promoting neurons, at high risk of oxidative damage1112.…”

mentioning

confidence: 99%

Contribution of sleep to the repair of neuronal DNA double-strand breaks: evidence from flies and mice

Bellesi

Bushey

Chini

et al. 2016

Sci Rep

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Exploration of a novel environment leads to neuronal DNA double-strand breaks (DSBs). These DSBs are generated by type 2 topoisomerase to relieve topological constrains that limit transcription of plasticity-related immediate early genes. If not promptly repaired, however, DSBs may lead to cell death. Since the induction of plasticity-related genes is higher in wake than in sleep, we asked whether it is specifically wake associated with synaptic plasticity that leads to DSBs, and whether sleep provides any selective advantage over wake in their repair. In flies and mice, we find that enriched wake, more than simply time spent awake, induces DSBs, and their repair in mice is delayed or prevented by subsequent wake. In both species the repair of irradiation-induced neuronal DSBs is also quicker during sleep, and mouse genes mediating the response to DNA damage are upregulated in sleep. Thus, sleep facilitates the repair of neuronal DSBs.

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Loss of Sleep Affects the Ultrastructure of Pyramidal Neurons in the Adolescent Mouse Frontal Cortex

Abstract: Ultrastructural analysis may be a powerful tool to identify which cellular organelles, and thus which cellular functions, are most affected by sleep and sleep loss.

Cited by 38 publications

References 63 publications

Sleep-deprived cognitive impairment in aging mice is alleviated by rapamycin

Sleep-deprived cognitive impairment in aging mice is alleviated by rapamycin

Molecular Mechanisms of Sleep Homeostasis in Flies and Mammals

Contribution of sleep to the repair of neuronal DNA double-strand breaks: evidence from flies and mice

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