Circadian VIPergic neurons of the suprachiasmatic nuclei sculpt the sleep-wake cycle
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA644912 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Although the mammalian rest-activity cycle is controlled by a "master clock" in the suprachiasmatic nuclei (SCN) of the hypothalamus, it is unclear how firing of individual SCN neurons gates individual features of daily activity. Here, we demonstrate that a specific transcriptomically identified population of mouse VIP+ SCN neurons is active at the "wrong" time of the day -nighttime- when most SCN neurons are silent. Using chemogenetic and optogenetic strategies, we show that these neurons and their cellular clocks are necessary and sufficient to gate and time nighttime sleep, but have no effect upon daytime sleep. We propose mouse nighttime sleep, analogous to the human siesta, is a "hard-wired" property gated by specific neurons of the master clock to favor subsequent alertness prior to dawn (a circadian "wake maintenance zone"). Thus, the SCN is not simply a 24h metronome: specific populations sculpt critical features of the sleep-wake cycle.
2021-01-21 | GSE154038 | GEO
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: Not available
| S-EPMC7803671 | biostudies-literature
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:22 healthy volunteers without sleep disorders were resident in an environmental scheduling facility and participated in a forced-desynchrony protocol, in which the sleep-wake cycle and the associated fasting-feeding cycle is scheduled to a 28-hour period, of which one third (i.e. 9h 20min) is scheduled for sleep. Under these conditions, during which light levels in the waking episode are kept low and sleep is scheduled in darkness, the phase of the melatonin rhythm occurred at approximately the same clock time during the first (D1) and fourth (D4) 28-h cycle and there were no major changes in either the amplitude or the waveform of this rhythm. During D1 and D4 7 blood samples were taken, RNA was extracted from leukocytes, labelled and hybridised to human whole-genome microarrays A total of 287 samples comprising 22 human subjects, for which 14 samples across multiple time-points/sleep condition were collected.
2014-01-23 | E-GEOD-48113 | biostudies-arrayexpress
Project description:Alignment of fasting and feeding with the sleep/wake cycle is coordinated by hypothalamic neurons, though the underlying molecular programs remain incompletely understood. Here we demonstrate that the clock transcription pathway maximizes eating during wakefulness and glucose production during sleep through transcription pathway maximizes eating during autonomous circadian regulation of NPY/AgRP neurons. Tandem profiling of whole cell and ribosome-bound mRNAs in morning and evening under dynamic fasting and fed conditions identified temporal control of activity-dependent gene repertoires in AgRP neurons central to synaptogenesis, bioenergetics, and neurotransmitter and peptidergic signaling. Synaptic and circadian pathways were specific to whole cell RNA analyses, while bioenergetic pathways were selectively enriched in the ribosome-bound transcriptome. Finally, we demonstrate that the AgRP clock mediates the transcriptional food acquisition with sleep/wake state. response to leptin. Our results reveal that time-of-day restriction in transcriptional control of energy-sensing neurons underlies the alignment of hunger and day restriction in transcriptional control of energy-sensing neurons underlies the alignment of hunger and food acquisition with sleep/wake state.
2019-03-04 | GSE124693 | GEO
Project description:Recent reports highlight phosphorylation as a major role in the regulation of sleep-wake cycles, to a lesser extent, the phosphoproteome in Suprachiasmatic Nucleus (SCN) is not well understood. We use multiplex tandem mass tag (TMT) - labelling coupled with liquid chromatography-mass spectrometry (LC-MS) to study the rhythmic regulatory effects of electroacupuncture(EA) at different times in constant darkness and the mechanism of EA mediated SCN protein phosphorylation. We applied the mass spectrometry-based phosphoproteome to explore the molecular characteristics of EA-induced phosphorylation modification in the SCN.
2021-10-31 | PXD029450 | iProX
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:22 healthy volunteers without sleep disorders were resident in an environmental scheduling facility and participated in a forced-desynchrony protocol, in which the sleep-wake cycle and the associated fasting-feeding cycle is scheduled to a 28-hour period, of which one third (i.e. 9h 20min) is scheduled for sleep. Under these conditions, during which light levels in the waking episode are kept low and sleep is scheduled in darkness, the phase of the melatonin rhythm occurred at approximately the same clock time during the first (D1) and fourth (D4) 28-h cycle and there were no major changes in either the amplitude or the waveform of this rhythm. During D1 and D4 7 blood samples were taken, RNA was extracted from leukocytes, labelled and hybridised to human whole-genome microarrays
2014-01-23 | GSE48113 | GEO
Project description:Analysis of the effects of sleep deprivation, recovery sleep, and three time-of-day controls on seven brain regions laser microdissected from mouse brain. The regions include the locus coeruleus, suprachiasmatic nucleus, hypocretin area, tuberomammillary nucleus, orbital cortex, posteromedial cortical amygdala, and entorhinal cortex.
2010-08-17 | GSE23628 | GEO