Microglia protect memories formed during sleep deprivation
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE174231 | GEO | 2021/05/12
REPOSITORIES: GEO
Similar Datasets
Project description:Microglia protect memories formed during sleep deprivation
| PRJNA728892 | ENA
Project description:The sleep-wake cycle is determined by a circadian and a sleep homeostatic process. However, the molecular impact of these two processes and their interaction on different cell populations in the brain remain unknown. To fill this gap, we have profiled the single-cell transcriptome of adult fruit fly brains across the sleep-wake cycle and different circadian times. We show cell type-specific transcriptomic changes between sleep/wakefulness states, different levels of sleep drive, and varying circadian times, with glial cells displaying the largest variations. Furthermore, the cell types whose transcriptomic dynamics correlate with the sleep homeostat or circadian clock are largely non-overlapping, with the exception of glial cells. Diminishing the circadian clock only in glial cells impairs the homeostatic sleep rebound after sleep deprivation. These findings reveal a comprehensive picture of different effects of sleep homeostatic and circadian processes on different cell types and define glial cells as the interaction sites of these two processes to determine sleep-wake dynamics.
2023-11-29 | GSE221239 | GEO
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:In humans, a primate-specific variable-number tandem-repeat (VNTR) polymorphism (4 or 5 repeats 54 nt in length) in the circadian gene PER3 is associated with differences in sleep timing and homeostatic responses to sleep loss. We investigated the effects of this polymorphism on circadian rhythmicity and sleep homeostasis by introducing the polymorphism into mice and assessing circadian and sleep parameters at baseline and during and after 12 h of sleep deprivation (SD). Microarray analysis was used to measure hypothalamic and cortical gene expression. Circadian behavior and sleep were normal at baseline. The response to SD of 2 electrophysiological markers of sleep homeostasis, electroencephalography (EEG) M-NM-8 power during wakefulness and M-NM-4 power during sleep, were greater in the Per35/5 mice. During recovery, the Per35/5 mice fully compensated for the SD-induced deficit in M-NM-4 power, but the Per34/4 and wild-type mice did not. Sleep homeostasis-related transcripts (e.g., Homer1, Ptgs2, and Kcna2) were differentially expressed between the humanized mice, but circadian clock genes were not. These data are in accordance with the hypothesis derived from human data that the PER3 VNTR polymorphism modifies the sleep homeostatic response without significantly influencing circadian parameters.-Hasan, S., van der Veen, D. R., Winsky-Sommerer, R., Hogben, A., Laing, E. E., Koentgen, F., Dijk, D.-J., Archer, S. N. A human sleep homeostasis phenotype in mice expressing a primate-specific PER3 variable-number tandem-repeat coding-region polymorphism. Mice recievied 12 hours of sleep restriction during the 12 hours of light in the light-dark cycle Boxhill represents Per35/5 mice and Coach represents Per34/4 mice. A total of 48 samples comprising 24 mice
2014-03-11 | E-GEOD-55494 | biostudies-arrayexpress
Project description:In humans, a primate-specific variable-number tandem-repeat (VNTR) polymorphism (4 or 5 repeats 54 nt in length) in the circadian gene PER3 is associated with differences in sleep timing and homeostatic responses to sleep loss. We investigated the effects of this polymorphism on circadian rhythmicity and sleep homeostasis by introducing the polymorphism into mice and assessing circadian and sleep parameters at baseline and during and after 12 h of sleep deprivation (SD). Microarray analysis was used to measure hypothalamic and cortical gene expression. Circadian behavior and sleep were normal at baseline. The response to SD of 2 electrophysiological markers of sleep homeostasis, electroencephalography (EEG) M-NM-8 power during wakefulness and M-NM-4 power during sleep, were greater in the Per35/5 mice. During recovery, the Per35/5 mice fully compensated for the SD-induced deficit in M-NM-4 power, but the Per34/4 and wild-type mice did not. Sleep homeostasis-related transcripts (e.g., Homer1, Ptgs2, and Kcna2) were differentially expressed between the humanized mice, but circadian clock genes were not. These data are in accordance with the hypothesis derived from human data that the PER3 VNTR polymorphism modifies the sleep homeostatic response without significantly influencing circadian parameters.-Hasan, S., van der Veen, D. R., Winsky-Sommerer, R., Hogben, A., Laing, E. E., Koentgen, F., Dijk, D.-J., Archer, S. N. A human sleep homeostasis phenotype in mice expressing a primate-specific PER3 variable-number tandem-repeat coding-region polymorphism. Mice were kept under 3.5h light- 3.5 hours dark cycles and samples were collected in the 17th light cycle Boxhill represents Per35/5 mice and Coach represents Per34/4 mice. A total of 30 samples comprizing 30 mice
2014-03-11 | E-GEOD-55495 | 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. 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:This a model from the article:
Sleep deprivation in a quantitative physiologically based model of the ascending
arousal system.
Phillips AJ, Robinson PA. J Theor Biol
2008 Dec 21;255(4):413-23 18805427
,
Abstract:
A physiologically based quantitative model of the human ascending arousal system
is used to study sleep deprivation after being calibrated on a small set of
experimentally based criteria. The model includes the sleep-wake switch of
mutual inhibition between nuclei which use monoaminergic neuromodulators, and
the ventrolateral preoptic area. The system is driven by the circadian rhythm
and sleep homeostasis. We use a small number of experimentally derived criteria
to calibrate the model for sleep deprivation, then investigate model predictions
for other experiments, demonstrating the scope of application. Calibration gives
an improved parameter set, in which the form of the homeostatic drive is better
constrained, and its weighting relative to the circadian drive is increased.
Within the newly constrained parameter ranges, the model predicts repayment of
sleep debt consistent with experiment in both quantity and distribution,
asymptoting to a maximum repayment for very long deprivations. Recovery is found
to depend on circadian phase, and the model predicts that it is most efficient
to recover during normal sleeping phases of the circadian cycle, in terms of the
amount of recovery sleep required. The form of the homeostatic drive suggests
that periods of wake during recovery from sleep deprivation are phases of
relative recovery, in the sense that the homeostatic drive continues to converge
toward baseline levels. This undermines the concept of sleep debt, and is in
agreement with experimentally restricted recovery protocols. Finally, we compare
our model to the two-process model, and demonstrate the power of physiologically
based modeling by correctly predicting sleep latency times following deprivation
from experimental data.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Phillips AJ, Robinson PA. (2008) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230115 | BioModels
Project description:This a model from the article:
Sleep deprivation in a quantitative physiologically based model of the ascending
arousal system.
Phillips AJ, Robinson PA. J Theor Biol
2008 Dec 21;255(4):413-23 18805427
,
Abstract:
A physiologically based quantitative model of the human ascending arousal system
is used to study sleep deprivation after being calibrated on a small set of
experimentally based criteria. The model includes the sleep-wake switch of
mutual inhibition between nuclei which use monoaminergic neuromodulators, and
the ventrolateral preoptic area. The system is driven by the circadian rhythm
and sleep homeostasis. We use a small number of experimentally derived criteria
to calibrate the model for sleep deprivation, then investigate model predictions
for other experiments, demonstrating the scope of application. Calibration gives
an improved parameter set, in which the form of the homeostatic drive is better
constrained, and its weighting relative to the circadian drive is increased.
Within the newly constrained parameter ranges, the model predicts repayment of
sleep debt consistent with experiment in both quantity and distribution,
asymptoting to a maximum repayment for very long deprivations. Recovery is found
to depend on circadian phase, and the model predicts that it is most efficient
to recover during normal sleeping phases of the circadian cycle, in terms of the
amount of recovery sleep required. The form of the homeostatic drive suggests
that periods of wake during recovery from sleep deprivation are phases of
relative recovery, in the sense that the homeostatic drive continues to converge
toward baseline levels. This undermines the concept of sleep debt, and is in
agreement with experimentally restricted recovery protocols. Finally, we compare
our model to the two-process model, and demonstrate the power of physiologically
based modeling by correctly predicting sleep latency times following deprivation
from experimental data.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Phillips AJ, Robinson PA. (2008) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230110 | BioModels
Project description:The circadian clock drives daily changes of physiology, including sleep-wake cycles, by regulating transcription, protein abundance and function. Circadian phosphorylation controls cellular processes in peripheral organs, but little is known about its role in brain function and synaptic activity. We applied advanced quantitative phosphoproteomics to mouse forebrain synaptoneurosomes isolated across 24h, accurately quantifying almost 8,000 phosphopeptides. Remarkably, half of the synaptic phosphoproteins, including numerous kinases, had large-amplitude rhythms peaking at rest-activity and activity-rest transitions. Bioinformatic analyses revealed global temporal control of synaptic function via phosphorylation, including synaptic transmission, cytoskeleton reorganization and excitatory/inhibitory balance. Remarkably, sleep deprivation abolished 98% of all phosphorylation cycles in synaptoneurosomes, indicating that sleep-wake cycles rather than circadian signals are main drivers of synaptic phosphorylation, responding to both sleep and wake pressures.
2019-10-14 | PXD010697 | Pride
Project description:In humans, a primate-specific variable-number tandem-repeat (VNTR) polymorphism (4 or 5 repeats 54 nt in length) in the circadian gene PER3 is associated with differences in sleep timing and homeostatic responses to sleep loss. We investigated the effects of this polymorphism on circadian rhythmicity and sleep homeostasis by introducing the polymorphism into mice and assessing circadian and sleep parameters at baseline and during and after 12 h of sleep deprivation (SD). Microarray analysis was used to measure hypothalamic and cortical gene expression. Circadian behavior and sleep were normal at baseline. The response to SD of 2 electrophysiological markers of sleep homeostasis, electroencephalography (EEG) θ power during wakefulness and δ power during sleep, were greater in the Per35/5 mice. During recovery, the Per35/5 mice fully compensated for the SD-induced deficit in δ power, but the Per34/4 and wild-type mice did not. Sleep homeostasis-related transcripts (e.g., Homer1, Ptgs2, and Kcna2) were differentially expressed between the humanized mice, but circadian clock genes were not. These data are in accordance with the hypothesis derived from human data that the PER3 VNTR polymorphism modifies the sleep homeostatic response without significantly influencing circadian parameters.-Hasan, S., van der Veen, D. R., Winsky-Sommerer, R., Hogben, A., Laing, E. E., Koentgen, F., Dijk, D.-J., Archer, S. N. A human sleep homeostasis phenotype in mice expressing a primate-specific PER3 variable-number tandem-repeat coding-region polymorphism.
2014-03-11 | GSE55494 | GEO