Ventral hippocampal transcriptome analysis after acute corticosterone exposure.
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ABSTRACT:
PROVIDER: PRJNA767042 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16100844.fastq.gz | Fastqsanger.gz | |||
| SRR16100845.fastq.gz | Fastqsanger.gz | |||
| SRR16100846.fastq.gz | Fastqsanger.gz | |||
| SRR16100847.fastq.gz | Fastqsanger.gz | |||
| SRR16100848.fastq.gz | Fastqsanger.gz |
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Project description:Aim: We investigated the effect of acute corticosterone exposure 3 hours after subcutaneous injection on the ventral hippocampus transcriptome. Methods: Adult male mice were used in the experiment. Mice were sacrificed 3 hours after corticosterone (3mg/kg) of vehicle injection and the ventral hippocampus was dissected and snap-frozen. Subsequently, total RNA was isolated and send for 100bp paired-end sequencing by BGI.
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Project description:Angelman Syndrome (AS) is a severe neurodevelopmental disorder, caused by the neuronal absence of the ubiquitin protein ligase E3A (UBE3A). UBE3A promotes ubiquitin-mediated protein degradation and functions as a transcriptional coregulator of nuclear hormone receptors, including the glucocorticoid receptor (GR). Previous studies showed anxiety-like behavior and hippocampal-dependent memory disturbances in AS mouse models. Hippocampal GR is an important regulator of the stress response and memory formation, and we therefore investigated whether the absence of UBE3A in AS mice disrupted GR signaling in the hippocampus. We first established a strong cortisol-dependent interaction between the GR ligand binding domain and a UBE3A nuclear receptor box in a high-throughput interaction screen. In vivo, we found that UBE3A-deficient AS mice displayed significantly more variation in circulating corticosterone levels throughout the day compared to wildtypes (WT), with low to undetectable levels of corticosterone at the trough of the circadian cycle. Additionally, we observed an enhanced transcriptomic response in the AS hippocampus following acute corticosterone treatment. Surprisingly, chronic corticosterone treatment showed less contrast between AS and WT mice in the hippocampus and liver transcriptomic responses. This suggests that UBE3A limits the acute stimulation of GR signaling, likely as a member of the GR transcriptional complex. Altogether, these data indicate that AS mice are more sensitive to acute glucocorticoid exposure in the brain compared to WT mice. This suggests that stress responsiveness is altered in AS which could lead to anxiety symptoms.
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Project description:We explored sex-biased effects of the primary stress glucocorticoid hormone corticosterone on the miRNA expression profile in the rat hippocampus. Adult adrenalectomized (ADX) female and male rats received a single corticosterone (10 mg/kg) or vehicle injection and after 6 h, hippocampi were collected for miRNA, mRNA and Western blot analyses. miRNA profiling microarrays showed a basal sex-biased miRNA profile in ADX rat hippocampi. Additionally, acute corticosterone administration triggered a sex-biased differential expression of miRNAs derived from genes located in several chromosomes and clusters on the X and 6 chromosomes. Putative promoter analysis unveiled that most corticosterone-responsive miRNA genes contained motifs for either direct or indirect glucocorticoid actions in both sexes. The evaluation of transcription factors indicated that almost 50 % of miRNA genes sensitive to corticosterone in both sexes was under glucocorticoid receptor regulation. Transcription factor-miRNA regulatory network analyses identified several transcription factors that regulate, activate or repress miRNA expression. Validated target mRNA analysis of corticosterone-responsive miRNAs showed a more complex miRNA-mRNA interaction network in males compared to females. Enrichment analysis revealed that several hippocampal-relevant pathways were affected in both sexes, such as neurogenesis and neurotrophin signaling. The evaluation of selected miRNA targets from these pathways displayed a strong sex difference in the hippocampus of ADX-vehicle rats. Corticosterone treatment did not change the levels of the miRNA targets and their corresponding tested proteins. Our data indicate that corticosterone exerts a sex-biased effect on hippocampal miRNA expression, which may engage in sculpting the basal sex differences observed at higher levels of hippocampal functioning.
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Project description:It was our goal to discern the genomic signatures of the dorsal and ventral hippocampus, in both mle and female mice after exposure to exogenous corticosterone, an animal model that induces a blunted response to stress. In addition to wildtype mice, we used mice heterozygous for the single nucleotide polymorphism of the gene encoding for brain-derived neurotrophic factor, BDNF Val66Met, a mouse model that shows susceptibility to stress.
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Project description:The hippocampal response to acute corticosterone elevation is altered in a mouse model for Angelman syndrome
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Project description:Circuit and molecular architecture of a ventral hippocampal network
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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
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Project description:The aim of the experiment was to test the effect of elevated level of corticosterone on hippocampal transcriptome after 12 hours of treatment during active phase to mimic the effect of a day-long stress. Additionally, we also tested the decay time of transcriptomic response during resting period when the level of glucocorticoids returns to the baseline. Our study shows that transcriptomic responses to glucocorticoids are heterogenous in terms of the decay time with some genes displaying persistent changes in expression during 9 hours of rest.
2022-11-24 | GSE218508 | GEO
Project description:Chronic pain is one of the most significant and costly medical problems throughout the world. Recent evidence has confirmed the hippocampus as an active modulator of pain chronicity but the underlying mechanisms remain poorly defined. By means of in vivo electrophysiology together with chemogenetic and optogenetic manipulations in freely behaving mice, we identified a neural ensemble in the ventral hippocampal CA1 (vCA1) that showed inhibitory responses to noxious external stimuli, but not to innocuous stimuli. Following peripheral inflammation, this neuronal ensemble became responsive to innocuous stimuli and causally contributed to sensory hypersensitivity in inflammatory animals. Mimicking this inhibition of vCA1 neurons using chemogenetics in naïve mice induced chronic pain-like behavioral changes, whereas activating these vCA1 neurons in mice with chronic peripheral inflammation resulted in a striking reduction of pain-related behaviors. Pathway-specific manipulation of vCA1 projections to the basolateral amygdala (BLA) and infralimbic cortex (IL) showed that these pathways were differentially involved in pain modulation at different temporal stages of chronic inflammatory pain. These results confirm a crucial role of the ventral hippocampus and its circuits in modulating the development of chronic pain in mice.
2022-12-19 | PXD038416 | Pride
Project description:The composition of genomic mediators of glucocorticoids in brain remains elusive because of common problem of low statistical power of experiments and associated very low consistency of transcriptomic data. Other issues is underrepresentation of chronic experiments and interpretation of differentially expressed genes without understanding their contribution to the total transcriptomic activity. To fill existing gaps in knowledge we have performed a large transcriptomic experiment (48 mice in total) testing effects of prolonged treatment with corticosterone (5, 14 and 28 days) on hippocampal transcriptome (RNA sequencing) and, next, we have assessed the contribution of differentially expressed genes to total transcriptomic activity. The experiment showed that prolonged treatment with the corticosterone induced a set of transcriptomic effects that were replicable across treatment durations including genes relevant for human PTSD (Opalin, Pllp, Ttyh2, Lpar1) and prolonged stress in animals (Cnp, Fam163a, Fcrls, Tmem125). Part of affected genes is specific for oligodendrocytes, neurons, astrocytes, immune cells, vascular system and brain ventricles indicating that glucocorticoids may affect all components of the central nervous system. The data showed also that the largest changes in expression of corticosterone-responsive genes are restricted to genes that have relatively low expression level and small contribution to the overall pool of mRNAs in the hippocampus. As a result, even large change in terms of the number of affected genes leads to small change in the number of mRNA copies. This means, in turn, that the transcriptomic changes induced by corticosterone are a low-cost effects for the brain.
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