PhosphoRiboTrap sequencing data of chemogenetic MCH neuron activation
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PROVIDER: PRJNA609068 | ENA |
REPOSITORIES: ENA
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Project description:We report phosphoRiboTrap experiments result which aim to explore the nature of the cell types in the Median Eminence (ME) regulated as a consequene of chemogenetic MCH neuron activation. Control and MCH-hM3Dq mice were 12 hrs-fasted and i.p. injected with CNO (3 mg/kg), Arcuate (ARC) and median eminence expat were extracted for preciptation of S6-marked ribosomes from both groups of mice. Extracted RNA from Immunoprecipitated ribosomes (IP) and total tissue (ARC+ME) from each mouse were subjected to deep mRNA sequencing. By analyzing the overlap of genes enriched in the IP/Input of MCH neuron activated mice with previously identified cell types using single cell mRNA sequencing of cells in the mediobasal hypothalamus (Campbell et al., 2017), we identified gene clusters which were activated upon MCH neuron activation.
2020-05-07 | GSE146019 | GEO
Project description:In order to understand heterogeneity of MCH neurons, by using MCH-Cre dependent ZsGreen (fl/fl) reporter mice, we isolated nuclear from 16 hypothalami of 16 mice at the age of 16-18weeks. Through flow cytometry, we were able to distinguish ZsGreen positive nuclei, and collected puried MCH nuclei in suspension. Those nuclei suspension were subjected to single cell sequence by 10x™ GemCode™ Technology for further single nuleus mRNA analysis and unravel subclusters of MCH neurons
2020-05-07 | GSE146020 | GEO
Project description:Purpose: RNAseq analysis was carried out to investigate the alterd genes by chemogenetic activation of endogenous oxytocin in the superficial layer (laminae I-II) and deep layer (laminae III-VI) of the dorsal horn. Methods: At 120 min after the s.c. administration of Saline or CNO (1 mg/kg) (n=3, each), adult male oxytocin-hM3Dq-mCherry transgenic rats were decapitated immediately without being anesthetized. Spinal cords specimens including laminae I-II and III-VI were collected separately. Results: 254 genes in the laminae I-II, and 191 genes in the laminae III-VI of the dorsal horn were significantly altered after chemogenetic activation of endogenous oxytocin.
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Project description:Neuroimmune crosstalk is critical for intestinal and tissue homeostasis. Yet the role of molecularly distinct subsets of gut-innervating neurons in regulating the activity of gut immunocytes, and the mechanisms of this neuroimmune signaling remain unclear. Here, we performed a chemogenetic and flow cytometry-based analysis of mice targeting eight different peripheral neuron subsets to assess how gut immunocytes are altered following neural activation. We found that distinct neurons modulated discreet anatomical populations of immunocytes in the gut in ileum, cecum, and colon. Nos1+ neuron activation decreased the percentage of RORg+ ileal conventional CD4+ T cells, whereas ChAT+ neuron activation decreased ileal neutrophils. Trpv1+ neuron activation displayed the most robust immunomodulatory phenotype, causing downregulation of RORg+ T regulatory cells in the colon and cecum. The immune cells exhibited decreased proliferation, enhanced cell stress, and altered cell activation markers. Further genetic and pharmacological approaches showed that spinal afferent Trpv1+ neurons specifically decreased Treg cells by signaling via the neuropeptide CGRP. Our study provided a comprehensive understanding of neuro-immune interactions, revealing a role for mechanisms by which Trpv1+ neurons regulate gut Treg cells.
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Project description:We sequenced total 12 samples: 3 samples at day 0 without Insulin induction, 3 samples at day 0 with MCH treatment, 3 samples at day 2 after insulin induction, 3 samples at day 2 after insulin inducation and MCH treatment.
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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.
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Project description:The postnatal neurodevelopmental disorder Rett syndrome (RTT) is caused by mutations in the gene encoding Methyl-CpG-binding Protein 2 (MeCP2). Despite decades of research, it remains unclear how MeCP2 actually regulates transcription or why RTT features appear only 6-18 months after birth. We examined MeCP2 binding to methylated cytosine in the CH context (mCH, where H = A, C, or T) in the adult mouse brain and found that MeCP2 binds these mCH sites, influencing nucleosome positioning and transcription. Strikingly, this pattern is unique to the mature nervous system, as it requires the increase in mCH after birth to reveal differences in MeCP2 binding to mCG, mCH, and non-methylated DNA elements. This study provides insight into the molecular mechanism governing MeCP2 targeting and how this targeting might contribute to the delayed onset of RTT symptoms. MeCP2 ChIP-Seq were conducted from ~ 7-week-old hypothalamus tissues from Mecp2-/y; MECP2-EGFP mice.
2015-04-15 | E-GEOD-66868 | biostudies-arrayexpress