Identification of molecular markers for candidate sleep-promoting neurons in CeA using TRAP-seq
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE121888 | GEO | 2020/04/06
REPOSITORIES: GEO
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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
Project description:Identification of molecular markers for candidate sleep-promoting neurons in CeA using TRAP-seq
| PRJNA498969 | ENA
Project description:The central amygdala (CEA) is a brain region that consists of primarily GABAergic neurons. It has been widely investigated for its role in many innate and adaptive behaviors, such as appetitive and defensive behaviors. Despite the complex functions of CEA, the molecular diversity of CEA neurons has not been systemically examined. Here, we performed single-cell RNA-sequencing (scRNA-Seq) in the CEA to classify the molecularly defined neuron types in this region.
2023-02-03 | GSE213828 | GEO
Project description:To investigate the effects of rabies infection on neuronal gene expression, we compared gene profiles of rabies infected and non-infected GABAergic neurons in the Zebrafish olfactory bulb.
2022-07-07 | E-MTAB-11083 | 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:<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:This a model from the article:
A quantitative model of sleep-wake dynamics based on the physiology of the
brainstem ascending arousal system.
Phillips AJ, Robinson PA. J Biol Rhythms
2007 Apr;22(2):167-79 17440218
,
Abstract:
A quantitative, physiology-based model of the ascending arousal system is
developed, using continuum neuronal population modeling, which involves
averaging properties such as firing rates across neurons in each population. The
model includes the ventrolateral preoptic area (VLPO), where circadian and
homeostatic drives enter the system, the monoaminergic and cholinergic nuclei of
the ascending arousal system, and their interconnections. The human sleep-wake
cycle is governed by the activities of these nuclei, which modulate the
behavioral state of the brain via diffuse neuromodulatory projections. The model
parameters are not free since they correspond to physiological observables.
Approximate parameter bounds are obtained by requiring consistency with
physiological and behavioral measures, and the model replicates the human
sleep-wake cycle, with physiologically reasonable voltages and firing rates.
Mutual inhibition between the wake-promoting monoaminergic group and
sleep-promoting VLPO causes ;;flip-flop'' behavior, with most time spent in 2
stable steady states corresponding to wake and sleep, with transitions between
them on a timescale of a few minutes. The model predicts hysteresis in the
sleep-wake cycle, with a region of bistability of the wake and sleep states.
Reducing the monoaminergic-VLPO mutual inhibition results in a smaller
hysteresis loop. This makes the model more prone to wake-sleep transitions in
both directions and makes the states less distinguishable, as in narcolepsy. The
model behavior is robust across the constrained parameter ranges, but with
sufficient flexibility to describe a wide range of observed phenomena.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Phillips AJ, Robinson PA. (2007) - 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.
2024-09-02 | BIOMD0000000917 | BioModels
Project description:We used microarrays to detailed global expression of colorectal cancer cells that expressed high or low levels of carcinoembryonic antigen. CEA high and CEA low cells were purified from LoVo and xenograft tumor derived from colorectal cancer patient (xhCRC) and were used for RNA extraction.
2015-08-27 | E-GEOD-72398 | 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: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