Differential effects of duration of sleep fragmentation on spatial learning and synaptic plasticity in pubertal mice

Wallace, Eli; Kim, Do Young; Kim, Kye Min; Chen, Stephanie; Braden, B. Blair; Williams, Jeremy; Jasso, Kalene R.; Garcia, Alexandra N.; Rho, Jong M.; Bimonte‐Nelson, Heather A.; Maganti, Rama

doi:10.1016/j.brainres.2015.04.037

Cited by 25 publications

(29 citation statements)

References 47 publications

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“…More specifically, we found that a night of consolidated sleep was associated with better learning abilities the next morning among Val/Val carriers. Our results confirm previous animal models showing the specific effect of sleep fragmentation on memory (Tartar et al, 2006;Rolls et al, 2011;Wallace et al, 2015). However, this positive sleep-memory association was not observed among Met carriers.…”

Section: Discussionsupporting

confidence: 91%

“…Sleep consolidation and NREM SWA have been identified as having a crucial role in learning (Tartar et al, 2006;Yoo et al, 2007;Van Der Werf et al, 2009;Rolls et al, 2011;Wallace et al, 2015). In the present study, we observed that BDNF Val/ Met polymorphism moderates the association between memory and the sleep consolidation index, a variable integrating the number of awakenings, sleep efficiency, and the longest sleep bout.…”

Section: Discussionsupporting

confidence: 64%

“…Rodent studies suggest that sleep fragmentation, independently of sleep duration, impairs long-term potentiation and the ability to learn (Tartar et al, 2006;Wallace et al, 2015). Moreover, a minimal unit of uninterrupted sleep, or sleep bout, is necessary to improve nextday learning (Rolls et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

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BDNF Val66Met Polymorphism Interacts with Sleep Consolidation to Predict Ability to Create New Declarative Memories

Gosselin

Beaumont

Gagnon

et al. 2016

Journal of Neuroscience

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It is hypothesized that a fundamental function of sleep is to restore an individual's day-to-day ability to learn and to constantly adapt to a changing environment through brain plasticity. Brain-derived neurotrophic factor (BDNF) is among the key regulators that shape brain plasticity. However, advancing age and carrying the BDNF Met allele were both identified as factors that potentially reduce BDNF secretion, brain plasticity, and memory. Here, we investigated the moderating role of BDNF polymorphism on sleep and next-morning learning ability in 107 nondemented individuals who were between 55 and 84 years of age. All subjects were tested with 1 night of in-laboratory polysomnography followed by a cognitive evaluation the next morning. We found that in subjects carrying the BDNF Val66Val polymorphism, consolidated sleep was associated with significantly better performance on hippocampus-dependent episodic memory tasks the next morning (␤-values from 0.290 to 0.434, p Յ 0.01). In subjects carrying at least one copy of the BDNF Met allele, a more consolidated sleep was not associated with better memory performance in most memory tests (␤-values from Ϫ0.309 to Ϫ0.392, p values from 0.06 to 0.15). Strikingly, increased sleep consolidation was associated with poorer performance in learning a short story presented verbally in Met allele carriers (␤ ϭ Ϫ0.585, p ϭ 0.005). This study provides new evidence regarding the interacting roles of consolidated sleep and BDNF polymorphism in the ability to learn and stresses the importance of considering BDNF polymorphism when studying how sleep affects cognition.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 64%

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BDNF Val66Met Polymorphism Interacts with Sleep Consolidation to Predict Ability to Create New Declarative Memories

Gosselin

Beaumont

Gagnon

et al. 2016

Journal of Neuroscience

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“…20 In rats and mice, experimentally induced sleep fragmentation through different methods also induces deficits in spatial learning, and this is associated with reduced long-term potentiation in the hippocampus. [21][22][23] Together, this experimental evidence supports a critical role for a minimum REM or NREM sleep duration for proper memory consolidation. In contrast to our study, however, all these protocols to induce sleep fragmentation result in shorter total sleep, REM sleep, or NREM sleep durations.…”

Section: Discussionsupporting

confidence: 58%

Fragmentation of Rapid Eye Movement and Nonrapid Eye Movement Sleep without Total Sleep Loss Impairs Hippocampus-Dependent Fear Memory Consolidation

Lee

Katsuyama

Duge

et al. 2016

Sleep

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Study Objectives: Sleep is important for consolidation of hippocampus-dependent memories. It is hypothesized that the temporal sequence of nonrapid eye movement (NREM) sleep and rapid eye movement (REM) sleep is critical for the weakening of nonadaptive memories and the subsequent transfer of memories temporarily stored in the hippocampus to more permanent memories in the neocortex. A great body of evidence supporting this hypothesis relies on behavioral, pharmacological, neural, and/or genetic manipulations that induce sleep deprivation or stage-specific sleep deprivation. Methods:We exploit an experimental model of circadian desynchrony in which intact animals are not deprived of any sleep stage but show fragmentation of REM and NREM sleep within nonfragmented sleep bouts. We test the hypothesis that the shortening of NREM and REM sleep durations post-training will impair memory consolidation irrespective of total sleep duration. Results: When circadian-desynchronized animals are trained in a hippocampus-dependent contextual fear-conditioning task they show normal short-term memory but impaired long-term memory consolidation. This impairment in memory consolidation is positively associated with the post-training fragmentation of REM and NREM sleep but is not significantly associated with the fragmentation of total sleep or the total amount of delta activity. We also show that the sleep stage fragmentation resulting from circadian desynchrony has no effect on hippocampus-dependent spatial memory and no effect on hippocampusindependent cued fear-conditioning memory. Conclusions: Our findings in an intact animal model, in which sleep deprivation is not a confounding factor, support the hypothesis that the stereotypic sequence and duration of sleep stages play a specific role in long-term hippocampus-dependent fear memory consolidation.

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“…Electroencephalographic (EEG) electrode implantation was performed at postnatal day (P) 34‐36 for all animals as previously described . Briefly, mice were anesthetized with isoflurane (5% induction, 1‐2% maintenance).…”

Section: Methodsmentioning

confidence: 99%

Altered circadian rhythms and oscillation of clock genes and sirtuin 1 in a model of sudden unexpected death in epilepsy

et al. 2018

Self Cite

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Attenuated oscillation of several core clock genes correlates with, and may underlie, aberrant diurnal and circadian rest-activity and sleep-wake patterns observed in Kcna1-null mice. This could contribute to late complications in epilepsy, such as sudden unexpected death in epilepsy. Sirt1 may represent a useful therapeutic target for rescuing circadian clock gene rhythmicity and sleep patterns in epilepsy.

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Differential effects of duration of sleep fragmentation on spatial learning and synaptic plasticity in pubertal mice

Cited by 25 publications

References 47 publications

BDNF Val66Met Polymorphism Interacts with Sleep Consolidation to Predict Ability to Create New Declarative Memories

BDNF Val66Met Polymorphism Interacts with Sleep Consolidation to Predict Ability to Create New Declarative Memories

Fragmentation of Rapid Eye Movement and Nonrapid Eye Movement Sleep without Total Sleep Loss Impairs Hippocampus-Dependent Fear Memory Consolidation

Altered circadian rhythms and oscillation of clock genes and sirtuin 1 in a model of sudden unexpected death in epilepsy

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