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Different DNA methylation between hypothalamus paraventricular (PVH) and ventromedial (VMH) nuclei

ABSTRACT: The goal is to compare the DNA methylation patterns between ARH and PVH to examine to what extent DNA methylation is region specific in genome scale.

ORGANISM(S): Mus musculus

PROVIDER: GSE48197 | GEO | 2013/10/01

SECONDARY ACCESSION(S): PRJNA209715

REPOSITORIES: GEO

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Different DNA methylation between hypothalamus paraventricular (PVH) and ventromedial (VMH) nuclei

Project description:The goal is to compare the DNA methylation patterns between ARH and PVH to examine to what extent DNA methylation is region specific in genome scale. ARH and PVH were micro-dissected from mice brains. Each 7 pieces of ARH or PVH were pooled and used for DNA methylation comparison by methylation specific amplification microarray (MSAM). As a brief description of the MSAM: 500ng of genomic DNA was serially digested with SmaI and XmaI followed by an adaptor ligation and adaptor mediated PCR amplification and then cohybridization. Two-color cohybridizations were performed as paired comparison of PVH vs. ARH with two biological replicates including dye swap.

2013-10-01 | E-GEOD-48197 | biostudies-arrayexpress

Neural and molecular mechanisms underlying paraventricular hypothalamus as a visceral and somatic pain sorting center

Project description:Distinct representation of visceral and somatic pain by unique PVH neuronal ensembles and suggested that PVH as a pain sorting center that distinctly processes visceral and somatic pain, providing a new framework for comprehending how the brain processes nociceptive information and identifying potential molecular targets for specific pain processing.

2024-09-23 | GSE254504 | GEO

An excitatory ventromedial hypothalamus to paraventricular thalamus circuit that suppresses food intake.

Project description:It is well recognized that ventromedial hypothalamus (VMH) serves as a satiety center in the brain. However, the feeding circuit for the VMH regulation of food intake remains to be defined. Here, we combine fiber photometry, chemo/optogenetics, virus-assisted retrograde tracing, ChR2-assisted circuit mapping and behavioral assays to show that selective activation of VMH neurons expressing steroidogenic factor 1 (SF1) rapidly inhibits food intake, VMH SF1 neurons project dense fibers to the paraventricular thalamus (PVT), selective chemo/optogenetic stimulation of the PVT-projecting SF1 neurons or their projections to the PVT inhibits food intake, and chemical genetic inactivation of PVT neurons diminishes SF1 neural inhibition of feeding. We also find that activation of SF1 neurons or their projections to the PVT elicits a flavor aversive effect, and selective optogenetic stimulation of ChR2-expressing SF1 projections to the PVT elicits direct excitatory postsynaptic currents. Together, our data reveal a neural circuit from VMH to PVT that inhibits food intake.

| S-EPMC7728757 | biostudies-literature

Paraventricular hypothalamic RUVBL2 neurons suppress appetite by enhancing excitatory synaptic transmission in distinct neurocircuits

Project description:The paraventricular hypothalamus (PVH) is crucial for food intake control, yet the presynaptic mechanisms underlying PVH neurons remain unclear. Here, we show that RUVBL2 in the PVH is significantly reduced during energy deficit, and knockout (KO) of PVH RUVBL2 results in hyperphagic obesity in mice. RUVBL2-expressing neurons in the PVH (PVHRUVBL2) exert the anorexigenic effect by projecting to the arcuate hypothalamus, the dorsomedial hypothalamus, and the parabrachial complex. We further demonstrate that PVHRUVBL2 neurons form the synaptic connections with POMC and AgRP neurons in the ARC. PVH RUVBL2 KO impairs the excitatory synaptic transmission by reducing presynaptic boutons and synaptic vesicles near active zone. Finally, RUVBL2 overexpression in the PVH suppresses food intake and protects against diet induced obesity. Together, this study demonstrates an essential role for PVH RUVBL2 in food intake control, and suggests that modulation of synaptic plasticity could be an effective way to curb appetite and obesity.

2024-10-02 | GSE249791 | GEO

Expression of ventromedial hypothalamus (VMH) from electroconvulsive seizure (ECS) treated C57Bl/6 mice

Project description:The ventromedial nucleus of the hypothalamus (VMH) is thought to a satiety center and a potential target for anti-obesity therapy. Electroconvulsive seizure (ECS) therapy is highly effective in psychiatric diseases including depression, but also implicated beneficial effects on other neurological diseases. Although it has been reported that the neurons in the VMH are strongly activated by ECS stimulation, the effect of ECS in this hypothalamic subnucleus remains unknown. To address this issue, we investigated molecular changes in the VMH in response to ECS by utilizing a method of laser-capture microdissection coupled with microarray analysis, and examined behavioral effects of ECS via VMH activation. ECS significantly induced gene expression not only immediate-early genes such as Fos, Fosb and Jun, but also Bdnf, Adcyap1, and Hrh1 in the VMH after a single or repeated stimulus. Mice received one or 7 times shock of ECS and their brains were collected at 2 h (VMH_1stECS2h, VMH_7thECS2h) or 6 h after shock (VMH_1stECS6h, VMH_7thECS6h). The brains of sham-treated animals were collected at 2 h after treatment(VMH_sham). The VMH was microdissected from dehydrated brain sections, and its total RNA was extracted. RNA samples from two or three animals were pooled to minimize the impact of biological variance. After nucleotide amplification by the ovation amplification, the gene expression profiles were obtained by the Affymetrix microarray analysis. The microarray analysis was performed twice using different sets of animals.

2012-05-29 | E-GEOD-38311 | biostudies-arrayexpress

Expression of ventromedial hypothalamus (VMH) from electroconvulsive seizure (ECS) treated C57Bl/6 mice

2012-05-30 | GSE38311 | GEO

Gene expression in mouse ventromedial hypothalamus (VMH) after deletion of SIRT1 in SF1 neurons

Project description:VMH was dissected from 16-week-old mice with deletion of SIRT1 in SF1 neurons (Sf1-Cre; Sirt1loxP/loxP) and intact controls (Sirt1loxP/loxP) and fed on high calorie diet from 8 weeks of age.

2018-06-01 | GSE99564 | GEO

RNAseq of 6 Different Rat Brain Areas after Treatment with a GLP-1 Receptor Agonist

Project description:In this study, we compared the treatment with one of 2 GLP-1 receptor agonists, Liraglutide and Semaglutide on the gene expression in 6 different DIO rat brain areas known to express the GLP-1 receptor. DIO rats were treated with vehicle, liraglutide, semaglutide or weight-matched for 23 days and tissue from the brain areas LS, PVH, ARH, DMH, AP and NTS was obtained with LCM.

2020-03-26 | E-MTAB-8078 | biostudies-arrayexpress

Paraventricular hypothalamic RUVBL2 neurons suppress appetite by enhancing excitatory synaptic transmission in distinct neurocircuits [RNA-seq]

Project description:Synaptic plasticity has been shown to participate in control of energy homeostasis.The paraventricular hypothalamus (PVH) is crucial for satiety control, though the underlying synaptic mechanisms remain unclear. Here, we show that RUVBL2 in the PVH is significantly reduced during energy deficit, and knockout (KO) of PVH RUVBL2 leads to hyperphagic obesity. We further show that KO of PVH RUVBL2 impairs the excitatory synaptic transmission by reducing presynaptic boutons and altering synaptic vesicle distribution. Chromatin immunoprecipitation-sequencing (ChlP-seq) data show that RUVBL2 binds to the promoters of numerous genes related to synaptic plasticity, in particular synaptic vesicle and neuron axonogenesis. Meanwhile, RNA-seq data show significant changes in the expression of some genes in these two pathways. Together, this study demonstrates an essential role for PVH RUVBL2 in food intake control, and suggests that modulating synaptic plasticity could be an effective way to curb appetite and obesity.

2024-10-02 | GSE252308 | GEO

Genome-wide analysis of gene expression in the paraventricular nucleus of Sim1-Cre specific DNMT3a deletion mice.

Project description:Analysis of gene expression in the paraventricular nucleus in the hypothalamus (PVH) of WT and Sim1-Cre specific DNMT3a deletion mice. Results provide important information about genes regulated by DNMT3a. For the gene expression profiling, total RNA was extracted from PVH of WT and Sim1-Cre specific DNMT3a deletion mice (C57BL6 background) at 6 weeks old using Qiagen RNeasy Lipid Tissue Mini Kit (Qiagen) and Phase Lock Gel (5 Prime Inc., Gaitherburg, MD). To make sure reproducibility and biological significance, triple hybridizations were performed for each genotype with the RNA from 3 indipendent PVH samples, each sample contains RNA from 5 animals. Genomics and Microarray Core Facility at UTSW (http://microarray.swmed.edu/) checked RNA quality with Bioanalyzer Chip and processed the samples for hybridization with Illumina Mouse-6 V2 BeadChip (Illumina Inc., San Diego, CA). We used GeneSpring GX (Agilent Technologies, Santa Clara, CA) for data analysis.

2014-09-01 | E-GEOD-42304 | biostudies-arrayexpress

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