Molecular correlates of sleep deprivation in the brain of three inbred mouse strains in an around-the-clock experiment
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE9442 | GEO | 2007/12/07
SECONDARY ACCESSION(S): PRJNA105157
REPOSITORIES: GEO
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Project description:These studies adress differential changes in gene expression between 6h sleep deprived and control mice in the brain and the liver. We profiled gene expression in three different inbred strains to understand the influence of genetic background. Keywords: brain, genetic background, sleep deprivation
2007-12-07 | GSE9441 | GEO
Project description:These studies adress differential changes in gene expression between 6h sleep deprived and control mice in the brain and the liver. We profiled gene expression in three different inbred strains to understand the influence of genetic background. Experiment Overall Design: Experiments were performed on male mice (C57BL/6J (B6), AKR/J (AK), DBA/2J (D2)), 12-13 weeks of aged, purchased from Jackson Laboratory. Animals were housed in a light/dark cycle of 24 hrs with water and food available ad libitum. Mice of the 3 inbred strains were sleep deprived for 6h starting at light onset (ZT0) and sacrificed together with their home-cage controls at ZT6 (n=9 / strain =3 / condition =2 / tissues =2; total = 108 mice).
2008-06-16 | E-GEOD-9441 | biostudies-arrayexpress
Project description:These studies adress differential changes in gene expression between sleep deprived and control mice. We profiled gene expression at four time points across the 24H Light/Dark cycle to take into account circadian influences and used three different inbred strains to understand the influence of genetic background. Experiment Overall Design: Experiments were performed on male mice ( AKR/J (A), C57BL/6J (B), DBA/2J (D)), 12-13 weeks of age, purchased from Jackson Laboratory. Animals were housed in a light/dark cycle of 24 hrs with water and food available ad libitum. Mice of the 3 inbred strains were sleep deprived for 6h starting at light onset (ZT0), at the middle of the light (ZT6), at the beginning of the dark (ZT12), or at the middle of the dark (ZT18) period, and sacrificed together with their home-cage controls (n=9 / strain =3 / time =4 / condition =2; total =216 mice).
2008-06-17 | E-GEOD-9442 | biostudies-arrayexpress
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:Inadequate sleep prevails in modern society and it impairs the circadian transcriptome. However, whether acute sleep deprivation has impact on the circadian rhythms is not clear. Here, we show that in mouse lung, a 10-hour acute sleep deprivation can alter the circadian expression of approximally 3,000 genes. We found that circadian rhythm disappears in genes related to metabolism and signaling pathways regulating protein phosphorylation after acute sleep deprivation, while the core circadian regulators do not change much in rhythmicity. Importantly, the strong positive correlation between mean expression and amplitude (E-A correlation) of cycling genes has been validated in both control and sleep deprivation conditions, supporting the energetic cost optimization model of circadian gene expression. Thus, we reveal that acute sleep deprivation leads to a profound change in the circadian gene transcription that influences the biological functions in lung.
2021-02-09 | GSE166335 | GEO
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:Purpose: To determine the specific effects of 6 hours sleep deprivation after a learning event on the transcriptomes of microglia. Sleep deprivation can generate inflammatory responses in the neuronal environment. In turn, this inflammation increases sleep drive, leading to a rebound in sleep duration. Microglia, a type of support cell found exclusively in the brain, have previously been found to release of inflammatory signals and exhibit altered characteristics in response to sleep deprivation. Together, this suggests microglia may be partially responsible for the brain’s response to sleep deprivation through their inflammatory activity. In this study, we fully and selectively ablated microglia from the mouse brain and assessed resulting sleep, circadian, and sleep deprivation phenotypes. We find microglia are dispensable for both homeostatic sleep and circadian function and the sleep rebound response to sleep deprivation. However, we uncover a phenomenon by which microglia appear to be essential for the protection of synapses and associated memories formed during a period of sleep deprivation, further expanding the list of known functions for microglia in synaptic modulation.
2021-05-12 | GSE174231 | GEO
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:Sleep deprivation (SD) performed before stroke induces an ischemic tolerance state as observed in other forms of preconditioning. As the mechanisms underlying this effect are not well understood we used DNA oligonucleotide microarray analysis, to identify the genes and the gene-pathways underlying SD preconditioning. Gene expression was analyzed 3 days after stroke surgery in four experimental groups: i) SD performed before focal cerebral ischemia induction; ii) SD performed before Sham surgery; iii) IS without SD; and iv) Sham surgery without SD. SD was performed by gentle handling during the last 6h of the light period and ischemia was induced immediately after. Stroke induced a massive alteration in gene expression both in sleep deprived and non-sleep deprived animals. However, compared to animals that underwent ischemia alone, SD induced a general reduction in transcriptional changes with a reduction in the upregulation of genes involved in cell cycle regulation and immune response. Moreover an upregulation of a new neuroendocrine pathway which included melanin concentrating hormone, glycoprotein hormones-M-kM-1-polypeptide and hypocretin was observed exclusively in rats sleep deprived before stroke. Our data indicate that SD before stroke reprogrammed the signaling response to injury. The inhibition of cell cycle regulation and inflammation are neuroprotective mechanisms reported also for other forms of preconditioning treatment whereas the implication of the neuroendocrine function is novel and has never been described before. These results therefore provide new insights into neuroprotective mechanisms involved in ischemic tolerance mechanisms.
2015-10-30 | E-MTAB-3148 | biostudies-arrayexpress
Project description:To gain insight into the molecular changes of sleep need, this study addresses gene expression changes in a subpopulation of neurons selectively activated by sleep deprivation. Whole brain expression analyses after 6h sleep deprivation clearly indicate that Homer1a is the best index of sleep need, consistently in all mouse strains analyzed. Transgenic mice expressing a FLAG-tagged poly(A)-binding protein (PABP) under the control of Homer1a promoter were generated. Because PABP binds the poly(A) tails of mRNA, affinity purification of FLAG-tagged PABP proteins from whole brain lysates, is expected to co-precipitate all mRNAs from neurons expressing Homer1a. Three other activity-induced genes (Ptgs2, Jph3, and Nptx2) were identified by this technique to be over-expressed after sleep loss. All four genes play a role in recovery from glutamate-induced neuronal hyperactivity. The consistent activation of Homer1a suggests a role for sleep in intracellular calcium homeostasis for protecting and recovering from the neuronal activation imposed by wakefulness. Experiment Overall Design: Experiments were performed on male mice, 12 weeks of age +/- 1 week. Animals were housed in polycarbonate cages (31x18x18cm) in an experimental room with an ambient temperature varying from 23° to 25°C under a 12:12 hrs light/dark cycle. Food and water were available ad libitum. At light onset mice were either sleep deprived by gentle handling (n=10) or left undisturbed (n=10) for 6 hrs. Animals were then randomly sacrificed by cervical dislocation. Total RNA from the whole brain was isolated for control (n=4) and sleep deprived (n=4) using a commercial RNA extraction kit (RNeasy Lipid Tissue Kit, Quiagen). Specific Homer1a-expressing cells polyA RNAs were immunoprecipitated following the total brain crosslinking (1% formaldehyde perfusion) for sleep deprived (n=6) and control (n=6) animals. The total RNA from the pull-down supernatants were also harvested (n=4). To test for transcriptional changes after sleep deprivation Homer1a-expressing cells, we proceeded in 2 steps: (1) identify probe sets enriched in the pull-down extracts, (2) among those probe sets compare sleep deprivation to control condition in both pull-down (6 vs. 6 chip comparison) and whole-brain (4 vs. 4 chip comparison) extracts. 4728 probe sets were significantly enriched at 5% FDR when pull-downs were compared to both supernatant and whole-brain extracts.
2008-06-16 | E-GEOD-9443 | biostudies-arrayexpress