Probing pathways by which rhynchophylline modifies sleep using spatial transcriptomics
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA896636 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22135104_1.fastq.gz | Fastqsanger.gz | |||
| SRR22135104_2.fastq.gz | Fastqsanger.gz | |||
| SRR22135105_1.fastq.gz | Fastqsanger.gz | |||
| SRR22135105_2.fastq.gz | Fastqsanger.gz | |||
| SRR22135106_1.fastq.gz | Fastqsanger.gz |
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Project description:Probing pathways by which rhynchophylline modifies sleep using spatial transcriptomics (additional files)
| PRJNA904265 | ENA
Project description:Here, we investigated the effects of Rhynchophylline (RHY) on the mouse brain spatial transcriptome. More precisely, we injected male and female mice intraperitoneally with either saline (NaCl) or RHY, either at Zeitgeber time (ZT referring to time in hour after light onset) 0 or at ZT0 and ZT11. Brains were sampled at ZT4 or ZT14, respectively, and immediately frozen embedded in OCT. Brains were treated and libraries were prepared according to 10x Genomics protocols for Visium Spatial Gene Expression. Sequencing was conducted by Genome Quebec (Montreal, Quebec, Canada). Findings reveal molecular routes by which RHY acts on the brain in a sleep-relevant context. Please cite the original paper when using these data (Ballester Roig et al., Biol Direct, 2023).
2023-05-05 | GSE217058 | GEO
Project description:Here, we investigated the effects of Rhynchophylline (RHY) on the mouse brain spatial transcriptome. More precisely, we injected male and female mice intraperitoneally with either saline (NaCl) or RHY, either at Zeitgeber time (ZT referring to time in hour after light onset) 0 or ZT0 and ZT11. Brains were sampled at ZT4 or ZT14, respectively, and immediately frozen embedded in OCT. Brains were treated and libraries were prepared according to 10x Genomics protocols for Visium Spatial Gene Expression. Sequencing was conducted by Genome Quebec (Montreal, Quebec, Canada). Findings reveal molecular routes by which RHY acts on the brain in a sleep-relevant context. Please cite the original paper when using these data (Ballester Roig et al., Biol Direct, 2023) and see also the submission GSE217058.
2023-05-05 | GSE218537 | GEO
Project description: Not available
| S-EPMC10161643 | biostudies-literature
Project description:We report a spatial transcriptomics dataset of mouse brain tissue generated with the 10x Genomics Visium platform to identify gene expression changes after sleep deprivation
2023-01-12 | GSE222410 | GEO
Project description:Sleep is governed by two processes: a circadian process that times sleep and wake and a homeostatic process that drives sleep as a function of prior wake history. Discovered in the fruit fly Drosophila, the period (per) gene is a “universal” cornerstone of the circadian clock, robustly oscillating at the transcript level, in all organs and tissues and in essentially all animals. We hypothesized that there may be a comparable factor (we term “sleeper”) for sleep homeostasis. To identify sleeper, we performed a wide-ranging transcriptomic analysis to identify genes whose expression tracks sleep-wake history in the Drosophila brain. We use a variety of methods to manipulate sleep-wake and subsequent rebound including mechanical, thermogenetic, optogenetic, pharmacological and circadian/baseline across 7 datasets. Using a log2 fold change threshold of 1, we did not identify any gene that was sleep-wake dependent across all datasets, raising the possibility that genes identified with a single method of sleep manipulation are related to the nature of the manipulation and not to sleep. Nonetheless, we identified genes whose expression changed with sleep-wake in a consistent direction across at least 2 datasets. We did observe significant pairwise overlap in regulated genes across many of the datasets. Gene ontology analysis of genes associated with sleep and wake as well as with sleep rebound. These analyses highlight previous processes implicated in sleep homeostasis as well as provide potentially novel pathways. In addition, we also examine genes whose expression correlates with prior sleep-wake history and/or predicted subsequent sleep rebound across these datasets. Among significantly correlated genes we observed some that were correlated with recent (<3h) sleep history while others were correlated with much longer (>6h) time frames suggesting temporally distinct genetic pathways for integrating waking experience. This analysis also highlights specific GO pathways for sleep/wake/rebound. Applying a novel GPT based paper search algorithm, we call fl.ai, we identified several genes with implicated or demonstrated function in sleep regulation consistent with potential homeostatic function. Collectively, these studies inform the future design of studies on the nature of sleep homeostasis as well as provide unique molecular clues across diverse sleep-wake conditions.
2026-06-07 | GSE322542 | 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:Homeostatic scaling is a global form of synaptic plasticity used by neurons to adjust overall synaptic weight and maintain neuronal firing rates while protecting information coding. While homeostatic scaling has been demonstrated in vitro, a clear physiological function of this plasticity type has not been defined. Sleep is an essential process that modifies synapses to support cognitive functions such as learning and memory. Evidence suggests that information coding during wake drives synapse strengthening which is offset by weakening of synapses during sleep .Here we use biochemical fractionation, proteomics and in vivo two-photon imaging to characterize wide-spread changes in synapse composition in mice through the wake/sleep cycle. We find that during the sleep phase, synapses are weakened through dephosphorylation and removal of synaptic AMPA-type glutamate receptors (AMPARs) driven by the immediate early gene Homer1a and signaling from group I metabotropic glutamate receptors (mGluR1/5), consistent with known mechanisms of homeostatic scaling-down in vitro. Further, we find that these changes are important in the consolidation of contextual memories. While Homer1a gene expression is driven by neuronal activity during wake, Homer1a protein targeting to synapses serves as an integrator of arousal and sleep need through signaling by the wake-promoting neuromodulator noradrenaline (NA) and sleep-promoting modulator adenosine. During sleep or periods of increased sleep need Homer1a enters synapses where it remodels mGluR1/5 signaling complexes to promote AMPAR removal. Thus, we have characterized widespread changes occurring at synapses through the wake/sleep cycle and demonstrated that known mechanisms of homeostatic scaling-down previously demonstrated only in vitro are active in the brain during sleep to remodel synapses, contributing to memory consolidation.
2017-02-13 | PXD004537 | Pride
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:The preoptic area (POA) of the hypothalamus is known to be crucial for sleep generation, but the spatial intermingling of sleep- and wake-promoting neurons makes it difficult to dissect the sleep control circuit. Here we identified a population of POA sleep-promoting neurons based on their projection target. Using a lentivirus for retrograde labeling with channelrhodopsin-2 (ChR2) followed by optogenetic manipulation and recording, we found that the POA GABAergic neurons projecting to the tuberomammillary nucleus (TMN) are both sleep active and sleep promoting. Cell type- and projection-specific rabies tracing revealed the presynaptic inputs to these neurons, including an amygdala GABAergic input that promotes wakefulness. Using single-cell RNA-seq, we identified several molecular markers for these neurons, and optogenetic activation of the POA neurons labeled by these markers confirmed their sleep-promoting effects. Together, these findings define a group of sleep-promoting neurons functionally, anatomically, and genetically.
2017-05-23 | GSE79108 | GEO