Transcriptomic response of the arcuate nucleus to oral corticosterone treatment
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE128148 | GEO | 2019/04/01
REPOSITORIES: GEO
Similar Datasets
Project description:Transcriptomic response of the arcuate nucleus to oral corticosterone treatment
| PRJNA526550 | ENA
Project description:Male Sprague-Dawley rats 8 weeks old, were adrenalectomized, treated with 300ug/kg corticosterone or vehicle 3 days after surgery then sacrificed 1 hour later. Hippocampi were removed and RNA extracted and processed for sequencing at the Massachusetts General Hospital Nex-Generation Sequening Core. Includes 6 cort treated and 6 control biological replicates
2016-08-11 | E-GEOD-84249 | biostudies-arrayexpress
Project description:Corticosterone (CORT)-mediated adaptive plasticity improves animal fitness in stressful environments. Although it brings ecological benefits, the cost potentially constrains its expression and evolution. Revealing the factors affecting plasticity costs is of great ecological and evolutionary significance. Evidence indicates that both CORT and background colour can induce metabolic changes in animals, which in turn determine phenotypic plasticity. However, whether and/or how CORT and background colour jointly act on plastic responses has not been studied. Here, this question has been investigated in amphibian tadpoles (Microhyla fissipes) exposed to CORT at different background colours (white or black) using integrated morphological, histological, and transcriptomic analyses. The results showed that CORT exposure increased relative tail length, immune function, and metabolic maintenance (i.e., transcription of substrate catabolism and oxidative phosphorylation) at the expense of reduction in growth rate and skin melanin level. The black background also increased relative tail length and metabolic maintenance (i.e., transcription of oxidative phosphorylation) at the cost of reduction in growth rate, but increased skin melanin level. The expression of critical pigmentation genes indicated that black background activated a distinct and opposite pigmentation regulating route to CORT. Although there was no interactive effect of background colour and CORT on phenotypic and metabolic variations, their additive effects further impact the trade-off between somatic growth, metabolic maintenance, and pigmentation in terms of resource allocation. In conclusion, the individual and additive effects of background colour and CORT exposure on tadpole plasticity were revealed. These results likely provide new insights into the environmental adaptation of animals.
2021-06-28 | GSE147684 | GEO
Project description:A vicious cycle ensues whereby prolonged exposure to social stress causes increased production of glucocorticoids, leading to obesity even further. Understanding the role of glucocorticoids, the key element in the vicious circle, might be helpful to break the vicious circle. However, the mechanism by which glucocorticoids induce obesity remains elusive. Herein we find that administration of corticosterone (CORT) to mice promotes the proliferation and survival of intestinal cells, which might contribute to the longer small intestines and the elongated intestinal villi, thus leading to increased nutrient absorption and obesity in mice. RNA-seq was performed to analyze transcriptional alterations in small intestines and livers after CORT-treatment, indicating differentially expressed genes (DEGs) were enriched in several cell growth/death-associated signaling pathways. This study would provide novel therapeutic clues for stress or glucocorticoids-related obesity.
2022-11-07 | GSE214009 | GEO
Project description:Three groups of Wistar rats with different manipulated levels of corticosterone were used to identify corticosteroid-responsive genes in hippocampus: 1. rats were adrenalectomised (ADX) 2. In addition to ADX these rats were implanted with a subcutaneous pellet containing 20 mg corticosterone and 80% cholesterol (ADX + low CORT) 3. In addition to ADX and implantation of a corticosterone pellet, these rats received a subcutaneous injection with corticosterone (1 mg/kg bodyweight) three hours prior to decapitation ((ADX + low CORT) + acute high CORT). All 3 groups of rats were decapitated three days after ADX and their hippocampus was isolated. Hippocampal RNA from 6 rats per group was pooled and used as input material for the SAGE libraries. Keywords: parallel sample
2003-10-30 | E-GEOD-787 | biostudies-arrayexpress
Project description:Although glucocorticoids (GCs) are known to exert numerous effects in the hippocampus, their chronic regulatory functions remain poorly understood. Moreover, evidence is inconsistent regarding the longstanding hypothesis that chronic GC exposure promotes brain aging/Alzheimer's disease. Here, we adrenalectomized male F344 rats at 15-months-of-age, maintained them for 3 months with implanted corticosterone (CORT) pellets producing low or intermediate (glucocorticoid-receptor (GR)-activating) blood levels of CORT, and performed microarray/pathway analyses in hippocampal CA1. We defined the chronic GC-dependent transcriptome as 393 genes that exhibited differential expression between Intermediate- and Low-CORT groups. Short-term CORT (4 days) did not recapitulate this transcriptome. Functional processes/pathways overrepresented by chronic CORT-upregulated genes included learning/plasticity, differentiation, glucose metabolism and cholesterol biosynthesis, whereas processes overrepresented by CORT-downregulated genes included inflammatory/immune/glial responses and extracellular structure. These profiles indicate that GCs chronically activate neuronal/metabolic processes while coordinately repressing a glial axis of reactivity/inflammation. We then compared the GC-transcriptome with a previously-defined hippocampal aging transcriptome, revealing a high proportion of common genes. Although CORT and aging moved expression of some common genes in the same-direction, the majority were shifted in opposite directions by CORT and aging (e.g., glial inflammatory genes downregulated by CORT are upregulated with aging). These results contradict the hypothesis that GCs simply promote brain aging, and also suggest that the opposite-direction shifts during aging reflect resistance to CORT regulation. Therefore, we propose a new model in which aging-related GC resistance develops in some target pathways while GC overstimulation develops in others, together generating much of the brain aging phenotype. Forty male Fischer 344 rats aged 14-15 months (late mid-age) were either sham operated (n=10) or adrenalectomized (n=30) at Harlan, Inc. (Indianapolis) and shipped to University of Kentucky 7-10 d after surgery. Animals were allowed to acclimate for 2 weeks after receipt prior to pellet-implant and were provided with food and water ad lib. Adrenalectomized (ADX) animals were maintained on drinking water containing isotonic saline with 1% sucrose, and also given supplemental feed mash (standard chow mixed with water and warmed) and apple chunks, as well as subcutaneous injections of 1.25 mg corticosterone sulfate (Solu-DeltaCort, Pfizer). During pellet-implant surgery, subjects were anesthetized with isoflurane, placed on a warming pad, and a 3 cm2 area on the animal's flank was shaved and sterilized. A 1-cm incision was made through the skin to form a subcutaneous pocket. Each sham animal received an inert pellet. ADX animals were divided into two groups, low-dose animals (n = 20) received one 25 mg CORT pellet and intermediate-dose animals (n = 10) received one 200 mg CORT pellet (slow release pellets, Innovative Research of America, Sarasota, FL). Incisions were closed with wound clips (removed after 7-10 days). Following implant surgery, subjects were housed singly for 3 months prior to euthanasia at age 18 months. Low-dose animals continued to receive saline/ sucrose drinking water, but other supplementation (food mash, Solu-Delta CORT, apple chunks) was discontinued. One ADX animal was removed from the study for declining health. During the twelfth week, just prior to study termination, half of the ADX low-dose CORT subjects were given a short-term, high-dose regimen consisting of 4 daily IP injections of 5mg/d CORT (considered a relatively high dose- Makino et al., 1995). All animals were killed between 8 and 10 AM on the last two days of the study. After deep CO2 anesthesia and decapitation, trunk blood was collected for CORT radioimmunoassay and hippocampal CA1 brain tissue was dissected as described previously (Blalock et al., 2003) for microarray analysis (see below). Final treatment groups consisted of: 1) Sham (intact) control, 2) Low-CORT (ADX), 3) Intermediate-CORT (ADX), and 4) Low-CORT (ADX) + short-term high-dose injected (n=9-10/group).
2013-07-22 | E-GEOD-37618 | biostudies-arrayexpress
Project description:Drop-seq and single cell sequencing of mouse arcuate nucleus and median eminence
2017-02-06 | GSE90806 | GEO
Project description:Background: As a worldwide threat to mental health, depression affects about 322 million people globally. Recently, the role of gut microbiota dysbiosis on the pathogenesis of depression has received widespread attention, but the underlying mechanism remains elusive.Results: Corticosterone (CORT)-treated mice showed depressive-like behaviors, a reduction in hippocampal neurogenesis, and an altered composition of gut microbiota (GM). Fecal microbial transplantation (FMT) from CORT-treated mice transferred depressive-like phenotypes and their dominant GM, especially bifidobacterium and lactobacillus, to the recipients. Fecal metabolic profiling showed that the relative abundances of fecal ceramides were significantly increased in CORT-treated and the recipient mice. Metagenomic sequencing exposed that bifidobacterium and lactobacillus might be responsible for gut ceramides production in CORT-treated mice. We then found that treatment with ceramides via oral gavage was sufficient to recapitulate the depressive-like phenotypes in wild -type mice. Finally, RNA-sequencing data exposed that most of the differentially expressed genes (DEGs) between ceramides-treated mice and the control group were enriched in oxidative phosphorylation (OXPHOS) pathway. Conclusion: We conclude that chronic exposure to CORT leads to an altered GM composition and consequent ceramides production, thus leading to subtle mitochondrial OXPHOS dysfunction in hippocampus, which may contribute to the development of depressive disorders.
2024-04-01 | GSE229237 | GEO
Project description:Although glucocorticoids (GCs) are known to exert numerous effects in the hippocampus, their chronic regulatory functions remain poorly understood. Moreover, evidence is inconsistent regarding the longstanding hypothesis that chronic GC exposure promotes brain aging/Alzheimer's disease. Here, we adrenalectomized male F344 rats at 15-months-of-age, maintained them for 3 months with implanted corticosterone (CORT) pellets producing low or intermediate (glucocorticoid-receptor (GR)-activating) blood levels of CORT, and performed microarray/pathway analyses in hippocampal CA1. We defined the chronic GC-dependent transcriptome as 393 genes that exhibited differential expression between Intermediate- and Low-CORT groups. Short-term CORT (4 days) did not recapitulate this transcriptome. Functional processes/pathways overrepresented by chronic CORT-upregulated genes included learning/plasticity, differentiation, glucose metabolism and cholesterol biosynthesis, whereas processes overrepresented by CORT-downregulated genes included inflammatory/immune/glial responses and extracellular structure. These profiles indicate that GCs chronically activate neuronal/metabolic processes while coordinately repressing a glial axis of reactivity/inflammation. We then compared the GC-transcriptome with a previously-defined hippocampal aging transcriptome, revealing a high proportion of common genes. Although CORT and aging moved expression of some common genes in the same-direction, the majority were shifted in opposite directions by CORT and aging (e.g., glial inflammatory genes downregulated by CORT are upregulated with aging). These results contradict the hypothesis that GCs simply promote brain aging, and also suggest that the opposite-direction shifts during aging reflect resistance to CORT regulation. Therefore, we propose a new model in which aging-related GC resistance develops in some target pathways while GC overstimulation develops in others, together generating much of the brain aging phenotype.
2013-07-22 | GSE37618 | GEO
Project description:We report changes in GR and Pol II binding profiles genome-wide upon treatment with corticosterone (Cort) for 20 minutes, treatment with Cort for 20 minutes followed by hormone withdrawal for 40 minutes, 60 minutes continuous stimulation with Cort, and 60 minutes continuous stimulation with Dexamethasone (Dex). We examine GR binding upon following treatments: 0' Cort, 20' Cort, 60' Cort Pulsed, 60' Cort Constant; Pol II binding upon following treatments: 0' Cort, 20' Cort, 60' Cort Pulsed, 60' Cort Constant, 60' Dex Constant; Pol II binding upon Mock treatments simulating 0' Cort, 20' Cort, 60' Cort Pulsed, 60' Cort Constant; CTCF binding profile of untreated cells.
2015-02-12 | E-GEOD-61234 | biostudies-arrayexpress