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Molecular codes defining lateral hypothalamic sleep regulating neurons

ABSTRACT: Molecular codes defining lateral hypothalamic sleep regulating neurons

PROVIDER: PRJNA521659 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8555030.fastq.gz	Fastqsanger.gz
	SRR8555040.fastq.gz	Fastqsanger.gz
	SRR8555031.fastq.gz	Fastqsanger.gz
	SRR8555032.fastq.gz	Fastqsanger.gz
	SRR8555033.fastq.gz	Fastqsanger.gz

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Molecular codes defining lateral hypothalamic sleep regulating neurons

Project description:Hypothalamic hypocretin (HCRT) and melanin concentrating hormone (MCH) have multiple functions including sleep and metabolism. How these neuropeptides are produced and involved in divers functions remain unknown. We developed methods to sort and purify HCRT and MCH neurons from mouse hypothalamus. RNA-sequencing revealed key factors of fate determination for HCRT (Peg3, Ahr1, Six6, Nr2f2 and Prrx1) and MCH (Lmx1, Gbx2 and Peg3) neurons. Amongst these, loss of Peg3 in mice significantly reduces HCRT and MCH cell numbers while knock-down of Peg3 ortholog in zebrafish completely abolishes their expression resulting in a two fold increase in sleep. The transcriptome results were used to produce HCRT and MCH neurons from induced pluripotent stem cells (iPSCs) and ascorbic acid was found necessary for HCRT and BMP7 for MCH cell differentiation. Our results provide a platform to understand the development and expression of HCRT and MCH and their multiple functions in health and disease.

2019-09-01 | GSE126330 | GEO

Loss of Snord116 impacts lateral hypothalamus, sleep, and food-related behaviors

Project description:Imprinted genes are highly expressed in the hypothalamus, however whether specific imprinted genes affect hypothalamic neuromodulators and their functions is unknown. It has been suggested that Prader-Willi syndrome (PWS), a neurodevelopmental disorder caused by lack of paternal expression at the chromosome 15q11-q13, characterised with a hypothalamic insufficiency. Here we investigate the role of paternally expressed Snord116 gene within the context of sleep and metabolic abnormalities of PWS, and we report a novel role of this imprinted gene in the function and organisation of the two main neuromodulatory systems of the lateral hypothalamus (LH), namely the orexin (OX) and the melanin concentrating hormone (MCH). We observe that the dynamic between neuronal discharge in the LH and sleep-wake states of mice carrying the paternal deletion of the Snord116 (PWScrm+/p-) is compromised. This abnormal state-dependent neuronal activity is paralleled by a significant reduction of OX neurons in LH of mutants. Therefore, we propose that unbalance between OX- and MCH- expressing neurons in the LH of mutants reflects in a series of deficits manifested in the PWS, such as dysregulation of rapid eye movement (REM) sleep, food intake and temperature control.

2020-05-25 | GSE139524 | GEO

Sleep-active hypothalamic MCH-system modulates hippocampal synaptic plasticity and is vulnerable in early Alzheimer’s Disease

Project description:In Alzheimer’s disease (AD), pathophysiological changes in the hippocampus cause deficits in episodic memory formation, leading to cognitive impairment. Hippocampal hyperactivity and decreased sleep quality are associated with early AD, but their basis is poorly understood. We find that homeostatic mechanisms transiently counteract increased excitatory drive of hippocampal CA1 neurons in AppNL-G-F mice, but fail to stabilize it at control levels. Spatial transcriptomics (ST) analysis identifies the Pmch gene encoding Melanin-Concentrating Hormone (MCH) as part of the adaptive response in AppNL-G-F mice. Hypothalamic MCH peptide is produced in sleep-active lateral hypothalamic neurons that project to CA1 and modulate memory. We show that MCH downregulates synaptic transmission and modulates firing rate homeostasis in hippocampal neurons. Moreover, MCH reverses the increased excitatory drive of CA1 neurons in AppNL-G-F mice. Consistent with our finding that a reduced fraction of MCH-neurons is active in AppNL-G-F mice, these animals spend less time in rapid eye movement (REM) sleep. In addition, MCH-axons projecting to CA1 become progressively impaired in both AppNL-G-F mice and AD patients. Our findings identify the MCH-system as vulnerable in early AD and suggest that impaired MCH-system function contributes to aberrant excitatory drive and sleep defects, which can compromise hippocampal-dependent functions.

2023-09-07 | GSE225181 | GEO

Obesity Remodels Activity and Transcriptional State of a Lateral Hypothalamic Brake on Feeding

Project description:We demonstrate that high fat diet (HFD)-induced obesity alters the transcriptional state of lateral hypothalamic glutamate neurons in mice.

2019-05-02 | GSE130597 | GEO

Loss of Snord116 impacts lateral hypothalamus, sleep, and food-related behaviors

Project description:Loss of Snord116 impacts lateral hypothalamus, sleep, and food-related behaviors

| PRJNA580049 | ENA

Ambiguous genetic codes

Project description:Crammed, ambiguous genetic codes

| PRJEB9019 | ENA

Single cell transcriptomic analysis of the lateral hypothalamic area reveals molecularly distinct populations of inhibitory and excitatory neurons

Project description:We employed a droplet-based single cell RNA-sequencing (scRNA-seq) approach to develop a comprehensive census of molecularly distinct cell types in the mouse lateral hypothalamic area (LHA). In addition to 13 distinct non-neuronal cell populations, we define 15 distinct populations of glutamatergic and 15 distinct populations of GABAergic neurons, including both known and novel cell types. This comprehensive transcriptomic analysis of LHA cell types lays the groundwork for understanding the circuit-level underpinnings of LHA coordination of innate behavior.

2019-01-15 | GSE125065 | GEO

Obesity Remodels Activity and Transcriptional State of a Lateral Hypothalamic Brake on Feeding

Project description:Obesity Remodels Activity and Transcriptional State of a Lateral Hypothalamic Brake on Feeding

| PRJNA540713 | ENA

Effect of 12 hour sleep restriction on the transcriptome of mice carying a human Per3 polymorphism

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

Targeted single cell expression profiling identifies integrators of sleep and metabolic state

Project description:The fruit fly, Drosophila melanogaster, suppresses sleep in response to acute food deprivation, presumably to forage for food. This process is dependent on a single pair of neurons, termed the Lateral Horn Leucokinin (LHLK) neurons, that secrete the neuropeptide Leucokinin. These neurons signal to insulin producing cells and suppress sleep under periods of starvation. Here, we use single-cell sequencing of LHLK neurons to examine the transcriptional responses to starvation.

2024-09-27 | GSE272264 | GEO

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