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PROVIDER: PRJEB21443 | ENA |
REPOSITORIES: ENA
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Project description:Extended periods of waking result in physiological impairments in humans, rats, and flies. Sleep homeostasis, the increase in sleep observed following sleep loss, is believed to counter the negative effects of prolonged waking by restoring vital biological processes that are degraded during sleep deprivation. Sleep homeostasis, as with other behaviors, is influenced by both genes and environment. We report here that during periods of starvation, flies remain spontaneously awake but, in contrast to sleep deprivation, do not accrue any of the negative consequences of prolonged waking. Specifically, the homeostatic response and learning impairments that are a characteristic of sleep loss are not observed following prolonged waking induced by starvation. To identify the genes responsible for the protective effects of starvation we conducted transcription profiling of sleep deprived flies that accrue sleep debt compared to starved siblings that do not. Genes involved in lipid metabolism were highly enriched in our dataset of 84 differentially regulated transcripts. Follow up genetic studies established that 6 genes involved in lipid metabolism strongly influence sleep homeostasis. Two of these genes, brummer (bmm) and Lipid storage droplet 2 (Lsd2), are in the same lipolysis pathway but exert antagonistic effects on lipid storage. bmm mutant flies have excess fat stores and display a large homeostatic response following sleep deprivation. In contrast, Lsd2 mutant flies, which phenocopy aspects of starvation as measured by low triglyceride stores, do not exhibit a homeostatic response following sleep loss. Importantly, Lsd2 mutant flies are not learning impaired after sleep deprivation. These results provide the first genetic evidence, to our knowledge, that lipid metabolism plays an important role in regulating the homeostatic response and can protect against neuronal impairments induced by prolonged waking. Two-condition experiments: sleep deprived vs starved. RNA from 8 biological replicates for each condition was pooled in groups of 2 to create 4 samples. Each of the 4 samples is run in duplicate with untreated circadian matched controls.
2014-04-15 | E-GEOD-18550 | biostudies-arrayexpress
Project description:Extended periods of waking result in physiological impairments in humans, rats, and flies. Sleep homeostasis, the increase in sleep observed following sleep loss, is believed to counter the negative effects of prolonged waking by restoring vital biological processes that are degraded during sleep deprivation. Sleep homeostasis, as with other behaviors, is influenced by both genes and environment. We report here that during periods of starvation, flies remain spontaneously awake but, in contrast to sleep deprivation, do not accrue any of the negative consequences of prolonged waking. Specifically, the homeostatic response and learning impairments that are a characteristic of sleep loss are not observed following prolonged waking induced by starvation. To identify the genes responsible for the protective effects of starvation we conducted transcription profiling of sleep deprived flies that accrue sleep debt compared to starved siblings that do not. Genes involved in lipid metabolism were highly enriched in our dataset of 84 differentially regulated transcripts. Follow up genetic studies established that 6 genes involved in lipid metabolism strongly influence sleep homeostasis. Two of these genes, brummer (bmm) and Lipid storage droplet 2 (Lsd2), are in the same lipolysis pathway but exert antagonistic effects on lipid storage. bmm mutant flies have excess fat stores and display a large homeostatic response following sleep deprivation. In contrast, Lsd2 mutant flies, which phenocopy aspects of starvation as measured by low triglyceride stores, do not exhibit a homeostatic response following sleep loss. Importantly, Lsd2 mutant flies are not learning impaired after sleep deprivation. These results provide the first genetic evidence, to our knowledge, that lipid metabolism plays an important role in regulating the homeostatic response and can protect against neuronal impairments induced by prolonged waking.
2014-04-15 | GSE18550 | GEO
Project description:We used microarrays to detail the global programme of gene expression underlying the effect of sleep deprivation in the mouse hippocampus and identified distinct classes of regulated genes during this process. Hippocampal tissue was taken from sleep deprived mice and time-matched non-sleep-deprived control animals that were left undisturbed in their home cages during the sleep deprivation period for a total of 8 and 9 replicates per group. RNA was isolated and cDNA was synthesized from hippocampal tissue, and the sample from each animal was hybridized to a separate Affymetrix Mouse 430_2 microarray
2012-09-06 | E-GEOD-33302 | biostudies-arrayexpress
Project description:Analysis of brain of Canton-S females deprived of sleep by perturbations during their normal sleep period. Perturbation effect also assessed during their active period to control for its effect during sleep deprivation. Results suggest processes altered during prolonged wakefulness and during sleep.
2007-07-06 | E-GEOD-4174 | biostudies-arrayexpress
Project description:Why we sleep is still one of the most perplexing mysteries in biology. Strong evidence, however, indicates that sleep is necessary for normal brain function and that the need to sleep is a tightly regulated process. Surprisingly molecular mechanisms that determine the need to sleep are incompletely described. Moreover, very little is known about transcriptional changes that specifically accompany the accumulation and discharge of sleep need. In this study we present an integrated 2 cross-laboratory analysis of the effects of sleep deprivation (SD) in gene expression in the mouse cortex. We also evaluate changes in gene expression genome-wide following various lengths of subsequent recovery sleep. (RS). We demonstrate that changes in gene expression specifically linked to SD or RS, and not to technical factors (e.g. the assay used), requires a novel analysis methodology not previously utilized in the field of sleep research. Cortical samples from mice were analyzed, from groups that were sleep deprived, sleep deprived and allowed to recover for 1, 2, 3, or 6 hours, and circadian control animals that were not sleep deprived. The experimental protocol began at lights on (ZT0) with 13 mice: 1 sacrificed, 4 control mice left undisturbed, and 8 mice kept awake with gentle brushing when attempting to sleep. After 5 hours of sleep deprivation the mice were randomly assigned to recovery sleep or continued sleep deprivation, and at fixed intervals the mice were sacrificed, dissected and the left cortex retained. The experimental protocol was repeated 7 times, one animal per timepoint per experimental day, so that 7 independent experiments are represented for each timepoint. All animals were acclimated to the brushing and tapping on cages used during sleep deprivationfor 6 days, and dissections and tissue collection were performed by a single experimenter.
2016-09-07 | E-GEOD-78215 | biostudies-arrayexpress
Project description:<p>Chronic sleep loss profoundly impacts metabolic health and shortens lifespan, but studies of the mechanisms involved have focused largely on acute sleep deprivation. To identify metabolic consequences of chronically reduced sleep, we conducted unbiased metabolomics on heads of three adult Drosophila short-sleeping mutants with very different mechanisms of sleep loss: fumin (fmn), redeye (rye), and sleepless (sss). Common features included elevated ornithine and polyamines, with lipid, acyl-carnitine, and TCA cycle changes suggesting mitochondrial dysfunction. Studies of excretion demonstrate inefficient nitrogen elimination in adult sleep mutants, likely contributing to their polyamine accumulation. Increasing levels of polyamines, particularly putrescine, promote sleep in control flies but poison sleep mutants. This parallels the broadly enhanced toxicity of high dietary nitrogen load from protein in chronically sleep-restricted Drosophila, including both sleep mutants and flies with hyper-activated wake-promoting neurons. Together, our results implicate nitrogen stress as a novel mechanism linking chronic sleep loss to adverse health outcomes-and perhaps for linking food and sleep homeostasis at the cellular level in healthy organisms.</p>
2023-03-18 | MTBLS3318 | MetaboLights
Project description:To gain insight into the dynamic molecular processes that are altered during prolonged wakefulness and during sleep. We performed an RNA expression profiling study examining temporal changes in the brain of Drosophila in relationship to the duration of prior sleep or wakefulness. Our experimental design allowed us to determine whether genes identified as differentially regulated between sleep and wakefulness were up- or down-regulated in these states. Because stimulation of the experimental animal during the normal sleep period is used to prolong wakefulness in most experimental paradigms, the interpretation of the effects of prolonged wakefulness is confounded by the effect of the perturbation stimulus itself on the animal’s biology. We controlled for this effect in our experimental paradigm by examining gene expression changes in response to identical stimulation but during the animal’s normal wakefulness. The design of our study also allowed us to control for circadian variation in gene expression, since we compared sleeping and sleep deprived flies at the same diurnal time. Keywords: sleep deprivation, time course, stress response
2006-02-27 | GSE4174 | GEO
Project description:Although at the organismal level sleep is defined as a behavioral state, at the level of the cerebral cortex sleep has a distinct local and use-dependent aspect. This observation raises the question whether sleep is a functional property of a complex brain or occurs at the level of neuronal assemblies with populations that were active more during wakefulness needing more intense sleep to recover. Here we show that primary cortical cultures have the capacity to change between sleep- and wake-like states that share key signatures with their in vivo counterparts. Cortical cultures initially exhibit random firing activity that is gradually replaced by a M-bM-^@M-^\sleep-likeM-bM-^@M-^] synchronized burst-pause firing activity as neurons mature and make connections. When stimulated with excitatory neurotransmitters, transient tonic firing is observed, followed by the reappearance of a M-bM-^@M-^\sleep-likeM-bM-^@M-^] state. Besides electrophysiological similarities also the transcriptional profile of stimulated cortical cultures greatly resembles that of the cortex of sleep deprived animals. We then used our in vitro model to map the metabolic pathways activated by the M-bM-^@M-^\wake-likeM-bM-^@M-^] state and found evidence for increased lysolipid release, strongly suggesting that sleep plays a role in neuronal membrane homeostasis. With our in vitro model the cellular and molecular consequences of sleep loss and the genetic determinants of disturbed sleep can now be investigated in a dish. Keywords: stress response For the in vivo transcriptome analyses mice were sleep deprived for 6 hours and brain harvested immediately afterwards. For the in vitro analyses, cortical cultures were stimulated with a neurotransmitter cocktail and cells harvested 3 hours afterwards. Control mice were kept undisturbed in their home cage and control cultures were sham stimulated with water. Also, another set of sleep deprived mice as well as stimulated cultures were allowed to recover before being sampled the next day at the time of day at which sleep deprivation or stimulation started the day before).
2012-08-31 | E-GEOD-33491 | biostudies-arrayexpress
Project description:Our aim was to investigate whether and how changes in sleep influences microglial function in the brain. We chronically sleep deprived mice expressing humanized TREM2 common variant, and mice without TREM2 expression in the presence or absence of amyloid plaques (Aβ).
2023-05-05 | GSE225360 | GEO
Project description:These studies address temporal changes in gene expression during spontaneous sleep and extended wakefulness in the mouse cerebral cortex, a neuronal target for processes that control sleep; and the hypothalamus, an important site of sleep regulatory processes. We determined these changes by comparing expression in sleeping animals sacrificed at different times during the lights on period, to that in animals sleep deprived and sacrificed at the same diurnal time. Keywords: gene expression, temporal changes, brain, behavior, sleep,
2007-02-11 | GSE6514 | GEO