Next Generation Sequencing Facilitates Quantitative Analysis of SPS and Control Rats Model
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE153081 | GEO | 2022/06/30
REPOSITORIES: GEO
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Project description:Prolonged stress has adverse consequences for neurons in the hippocampus (HIPP). The amygdala (AMY) is a brain region that is similar to HIPP across many measures, suggesting that chronic stress might modulate AMY and HIPP function in similar ways. However, studies addressing this issue have produced surprising results. For example, a regimen of chronic stress shown to produce atrophy in HIPP neurons caused dendritic branching in AMY neurons. These and other data have revealed that excessive stress induces fundamentally opposing processes in the AMY and HIPP, such that AMY function is facilitated by levels of stress that produce deleterious effects in HIPP. The mechanisms that contribute to the opposing responses of these brain regions to chronic stress are unknown. Such knowledge may suggest novel directions for pharmacological interventions to protect the HIPP from stress-mediated damage.,We will determine gene expression patterns in the hippocampus and amygdala under basal and stressful conditions, with a particular interest in those genes that are differentially regulated across the two regions. ,We hypothesize that genes that are oppositely regulated in the amygdala and hippocampus after stress mediate the opposing functional consequences of chronic stress in these two brain regions. Moreover, genes which are differentially expressed in these regions under basal conditions may underlie the distinct responses of these regions to stress.,Rats will receive either 30sec of handling (Control group; n=15) or 3hr of immobilization stress (Stress group; n=15) each day for 14 consecutive days. This stress paradigm has previously been shown to produce opposing effects on dendritic morphology and region-dependent behaviors for the hippocampus versus amygdala. Twenty-four hours after the last stress or handling session, the rats will be overanaesthetized, and the brain will be removed and placed in ice-cold buffer. Tissue will be rapidly dissected from the basolateral complex of the amygdala and the CA3 region of the hippocampus of both hemispheres, flash frozen in liquid nitrogen, and stored at -80C until further processing. The tissue from each brain region will be pooled across groups, yielding four samples (Control-Hippocampus, Control-Amygdala, Stress-Hippocampus, and Stress-Amygdala). Total RNA will be extracted using standard methods, and sent to the centers. Each sample will be run in triplicate, utilizing a total of 12 Affymetrix Rat Genome U34A gene chips. A triplicate array assay of pooled samples has previously been shown to both substantially increase the sensitivity of detecting genes of interest and reduce the variability associated with individual microarrays. In addition, the large number of rats used in each group will reduce the variability in gene expression associated with individual responses to chronic stress, as well as variability due to slight anatomical differences in the tissue extracted from each rat.
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Project description:Delineating the molecular basis of individual differences in the stress response is critical to understanding the pathophysiology and treatment of posttraumatic stress disorder (PTSD). In this study, 7 d after predator-scent-stress (PSS) exposure, male and female rats were classified into vulnerable (i.e., M-bM-^@M-^\PTSD-likeM-bM-^@M-^]) and resilient (i.e.,minimally affected) phenotypes on the basis of their performance on a variety of behavioral measures. Genome-wide expression profiling in blood and two limbic brain regions (amygdala and hippocampus), followed by quantitative PCR validation, was performed in these two groups of animals, as well as in an unexposed control group. Differentially expressed genes were identified in blood and brain associated with PSS-exposure and with distinct behavioral profiles postexposure. There was a small but significant between-tissue overlap (4M-bM-^@M-^S21%) for the genes associated with exposure-related individual differences, indicating convergent gene expression in both sexes. To uncover convergent signaling pathways across tissue and sex, upstream activated/deactivated transcription factorswere first predicted for each tissue and then the respective pathways were identified. Glucocorticoid receptor (GR) signaling was the only convergent pathway associatedwith individual differences when using the most stringent statistical threshold. Total RNA obtained from hippocampus of rats exposed to predator-scent-stress and showing extreme (n=5 males and n=5 females) or minimal (n=5 males and n=5 females) behavioral response compared to unexposed to stress and behaviorally tested controls (n=5 males and n=5 females).
2014-09-08 | E-GEOD-60303 | biostudies-arrayexpress
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Project description:Posttraumatic stress disorder (PTSD) is a prevalent psychiatric disorder. Several studies have attempted to characterize molecular alterations associated with PTSD, but most findings were limited to the investigation of specific cellular markers in the periphery or defined brain regions. In the current study, we aimed to unravel affected molecular pathways/mechanisms in the fear circuitry associated with PTSD. We interrogated a foot shock induced-PTSD mouse model by integrating proteomics and metabolomics profiling data. Alterations at the proteome level were analyzed using in vivo 15N metabolic labeling combined with mass spectrometry in prelimbic cortex (PrL), anterior cingulate cortex (ACC), basolateral amygdala (BLA), central nucleus of amygdala (CeA) and CA1 of hippocampus between shocked and non-shocked (control) mice, with and without fluoxetine treatment.
2022-02-28 | PXD002288 | Pride
Project description:Posttraumatic stress disorder (PTSD) is a prevalent psychiatric disorder. Several studies have attempted to characterize molecular alterations associated with PTSD, but most findings were limited to the investigation of specific cellular markers in the periphery or defined brain regions. In the current study, we aimed to unravel affected molecular pathways/mechanisms in the fear circuitry associated with PTSD. We interrogated a foot shock induced PTSD mouse model by integrating proteomics and metabolomics profiling data. Alterations at the proteome level were analyzed using in vivo 15N metabolic labeling combined with mass spectrometry in prelimbic cortex (PrL), anterior cingulate cortex (ACC), basolateral amygdala (BLA), central nucleus of amygdala (CeA) and CA1 of hippocampus between shocked and non-shocked (control) mice, with and without fluoxetine treatment.
2018-10-17 | PXD002271 | Pride
Project description:Posttraumatic stress disorder (PTSD) is a prevalent psychiatric disorder. Several studies have attempted to characterize molecular alterations associated with PTSD, but most findings were limited to the investigation of specific cellular markers in the periphery or defined brain regions. In the current study, we aimed to unravel affected molecular pathways/mechanisms in the fear circuitry associated with PTSD. We interrogated a foot shock induced-PTSD mouse model by integrating proteomics and metabolomics profiling data. Alterations at the proteome level were analyzed using in vivo 15N metabolic labeling combined with mass spectrometry in prelimbic cortex (PrL), anterior cingulate cortex (ACC), basolateral amygdala (BLA), central nucleus of amygdala (CeA) and CA1 of hippocampus between shocked and non-shocked (control) mice, with and without fluoxetine treatment.
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Project description:To explored the mechanism of pharmacokinetic perturbation in chronic unpredicted mild stress (CUMS) resulting depression, CUMS-induced depression animal model with spontaneous diabetic GK rats were established. The expression profile in GK rats' livers were screened using Affymetrix Rat 230 2.0 Array.
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Project description:The chain of events leading from oxidation stress is still barely understood. With the emergence of high-throughput sequencing, it is now possible to discover many different biological components simultaneously. Using RNA-seq technology, we sequenced the complete transcriptome of hippocampus of Rongchang piglets exposed to iron dextran (FeDex) treatment, a potent inducer of oxidation stress. Total RNAs from hippocampus of Rongchang piglet were sequenced and 11.5 Gb sequencing data was obtained. This analysis revealed regulatory molecules involved in oxidation stress through the identification of 362 differentially expressed genes (DEGs) and the functional analysis of DEGs. Furthermore, 76 neuropeptide gene transcripts, 60 neuropeptide receptor gene transcripts, were identified in hippocampus of Rongchang piglets, even though mRNA levels of only six neuropeptide genes were significantly changed. Totally, by using the RNA-seq we elucidated for the first time the transcriptomic changes directly caused by the injection of iron dextran. This system enabled the characterization of the transcriptional response triggered by oxidation stress in hippocampus of Rongchang piglet.
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Project description:Purpose: To identify genes differentially expressed in parvalbumin-positive (PV) interneurons of the hippocampus in non-defetaed (CTRL), stress-susceptible and stress-resilient mice. Method: Translating Ribosome Affinity Purification (TRAP) to isolate RNA from PV+ cells, cDNA synthesis and next generation RNAseq using Illumina Nextseq 500 sequencer. Results: RNA-seq revealed 458 DEGs between non-defeated and resilient mice, 1976 DEGs in non-defeated and susceptible mice, and 3475 DEGs in resilient and susceptible mice.
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