Synaptic plasticity in sleep: learning, homeostasis and disease

Wang, Gordon; Grone, Brian P.; Colas, Damien; Appelbaum, Lior; Mourrain, Philippe

doi:10.1016/j.tins.2011.07.005

Cited by 149 publications

(105 citation statements)

References 138 publications

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“…Egr1 is implicated in the maintenance of synaptic plasticity and is necessary for the persistence of LTP [47] and the consolidation of different forms of long-term memory as well as during the transition SYNJ1 AIRN DLK1 EGR3 EGR1 FOS HOMER1 DBP PER2 PLAGL1 PEG10 PROK2 GF2R MTRNR2 NPTX2 EGR1 HOMER1 PER2 PEG10 PROK2 DLK1 DRD1A ATP10A STAT5A L3MBTL PDE10A ZIM1 SFMBT2 from short-to long-term memories [48,49]. Interestingly, sleep is significantly involved in the regulation of brain plasticity and cognition (see [50] for review). A series of studies have shown that PKA and CREB signalling pathways promote wakefulness [51].…”

Section: Resultsmentioning

confidence: 99%

Parent-of-origin genetic background affects the transcriptional levels of circadian and neuronal plasticity genes following sleep loss

Tinarelli

García-García

Nicassio

et al. 2014

Phil. Trans. R. Soc. B

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Sleep homoeostasis refers to a process in which the propensity to sleep increases as wakefulness progresses and decreases as sleep progresses. Sleep is tightly organized around the circadian clock and is regulated by genetic and epigenetic mechanisms. The homoeostatic response of sleep, which is classically triggered by sleep deprivation, is generally measured as a rebound effect of electrophysiological measures, for example delta sleep. However, more recently, gene expression changes following sleep loss have been investigated as biomarkers of sleep homoeostasis. The genetic background of an individual may affect this sleep-dependent gene expression phenotype. In this study, we investigated whether parental genetic background differentially modulates the expression of genes following sleep loss. We tested the progeny of reciprocal crosses of AKR/J and DBA/2J mouse strains and we show a parent-of-origin effect on the expression of circadian, sleep and neuronal plasticity genes following sleep deprivation. Thus, we further explored, by in silico , specific functions or upstream mechanisms of regulation and we observed that several upstream mechanisms involving signalling pathways (i.e. DICER1, PKA), growth factors (CSF3 and BDNF) and transcriptional regulators (EGR2 and ELK4) may be differentially modulated by parental effects. This is the first report showing that a behavioural manipulation (e.g. sleep deprivation) in adult animals triggers specific gene expression responses according to parent-of-origin genomic mechanisms. Our study suggests that the same mechanism may be extended to other behavioural domains and that the investigation of gene expression following experimental manipulations should take seriously into account parent-of-origin effects.

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Section: Resultsmentioning

confidence: 99%

Parent-of-origin genetic background affects the transcriptional levels of circadian and neuronal plasticity genes following sleep loss

Tinarelli

García-García

Nicassio

et al. 2014

Phil. Trans. R. Soc. B

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“…90 The synaptic downscaling hypothesis posits, in effect, that the previously characterized recalibration of synaptic strengths 90 does not suffice during wakefulness, and that sleep is required for a further downscaling. 26 Studies on a role of sleep in memory and the evidence for such a role [91][92][93][94][95] are also based on nonmolecular models, in part because we still do not know what exactly a long-term memory trace is. In sum, even if these plausible nonmolecular conjectures about sleep are eventually found to be correct in their domains, they would not, by themselves, identify the fundamental molecular problem that the function of sleep may have to address.…”

Section: Introductionmentioning

confidence: 99%

Augmented generation of protein fragments during wakefulness as the molecular cause of sleep: a hypothesis

Varshavsky

2012

Protein Science

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Despite extensive understanding of sleep regulation, the molecular-level cause and function of sleep are unknown. I suggest that they originate in individual neurons and stem from increased production of protein fragments during wakefulness. These fragments are transient parts of protein complexes in which the fragments were generated. Neuronal Ca 21 fluxes are higher during wakefulness than during sleep. Subunits of transmembrane channels and other proteins are cleaved by Ca 21 -activated calpains and by other nonprocessive proteases, including caspases and secretases. In the proposed concept, termed the fragment generation (FG) hypothesis, sleep is a state during which the production of fragments is decreased (owing to lower Ca 21 transients) while fragment-destroying pathways are upregulated. These changes facilitate the elimination of fragments and the remodeling of protein complexes in which the fragments resided. The FG hypothesis posits that a proteolytic cleavage, which produces two fragments, can have both deleterious effects and fitness-increasing functions. This (previously not considered) dichotomy can explain both the conservation of cleavage sites in proteins and the evolutionary persistence of sleep, because sleep would counteract deleterious aspects of protein fragments. The FG hypothesis leads to new explanations of sleep phenomena, including a longer sleep after sleep deprivation. Studies in the 1970s showed that ethanol-induced sleep in mice can be strikingly prolonged by intracerebroventricular injections of either Ca 21 alone or Ca 21 and its ionophore (Erickson et al., Science 1978;199:1219-1221 Harris, Pharmacol Biochem Behav 1979;10:527-534; Erickson et al., Pharmacol Biochem Behav 1980;12:651-656). These results, which were never interpreted in connection to protein fragments or the function of sleep, may be accounted for by the FG hypothesis about molecular causation of sleep.

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“…1,2 Sleep disruptions have been implicated in cognitive impairment and dementia, 3 thus providing a modifiable target for prevention strategies with significant public health implications.…”

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confidence: 99%

Obstructive sleep apnea and neurocognitive function in a Hispanic/Latino population

et al. 2015

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Synaptic plasticity in sleep: learning, homeostasis and disease

Cited by 149 publications

References 138 publications

Parent-of-origin genetic background affects the transcriptional levels of circadian and neuronal plasticity genes following sleep loss

Parent-of-origin genetic background affects the transcriptional levels of circadian and neuronal plasticity genes following sleep loss

Augmented generation of protein fragments during wakefulness as the molecular cause of sleep: a hypothesis

Obstructive sleep apnea and neurocognitive function in a Hispanic/Latino population

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