Gene expression in murine amygdala, cortex, hippocampus and hypothalamus of Pianp-deficient mice
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PROVIDER: PRJNA513493 | ENA |
REPOSITORIES: ENA
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Project description:Pianp (also known as Leda-1) is a type I transmembrane protein with preferential expression in the mammalian central nervous system. We used microarrays to analyze the programme of gene expression in murine brain regions amygdala, cortex, hippocampus and hypothalamus of Pianp deficient mice.
2019-09-06 | GSE124791 | GEO
Project description:Three brain regions of the limbic system, the amygdala, hippocampus and hypothalamus, are responsible for survival behaviors such as feeding and physical challenging. Hypothalamus works together with pituitary and adrenal gland (HPA-axis) to adjust homeostatic state by modulating stress-response hormones. Unraveling molecular signatures such as DNA methylation of these tissues may provide deeper insights into a link between epigenetic regulation and phenotypic plasticity of behavioral responses of animals. We examined the DNA methylation profile of amygdala (n = 20), hippocampus (n = 20), hypothalamus (n = 19) as well as a non-brain tissue, adrenal gland (n=19) of German Landrace pigs using a cost effective method, Reduced Representation Bisulfite Sequencing (RRBS).
2024-11-19 | E-MTAB-10640 | biostudies-arrayexpress
Project description:Wolfram syndrome is caused by mutations in the WFS1 gene. WFS1 protein dysfunction results in a range of neuroendocrine syndromes and is mostly characterized by juvenile-onset diabetes mellitus and optic atrophy. WFS1 has been shown to participate in membrane trafficking, protein processing and Ca2+ homeostasis in the endoplasmic reticulum. In the present study we aimed to find the transcriptomic changes influenced by Wfs1 in the hypothalamus and hippocampus using RNA-sequencing. We used WFS1-deficient mice as a model system to analyze the changes in transcriptional networks. The number of differentially expressed genes between hypothalami of WFS1-deficient (Wfs1KO) and wild-type (WT) mice was 43 and between hippocampi 311 with False Discovery Rate (FDR) <0.05. In hypothalamus of Wfs1KO mice one of the most upregulated genes was Avpr1a whilst Avpr1b was significantly upregulated in hippocampus. Trpm8 was the most upregulated gene in the hippocampus of Wfs1KO mice. The functional analysis revealed significant enrichment of networks and pathways associated with protein synthesis, cell-to-cell signaling and interaction, molecular transport, metabolic disease and nervous system development and function. In conclusion, the transcriptomic profiles of WFS1-deficient hypothalamus and hippocampus do indicate the activation of degenerative molecular pathways causing the clinical occurrences typical to Wolfram syndrome.
2017-12-01 | GSE102624 | GEO
Project description:Wolfram syndrome is caused by mutations in the WFS1 gene. WFS1 protein dysfunction results in a range of neuroendocrine syndromes and is mostly characterized by juvenile-onset diabetes mellitus and optic atrophy. WFS1 has been shown to participate in membrane trafficking, protein processing and Ca2+ homeostasis in the endoplasmic reticulum. In the present study we aimed to find the transcriptomic changes influenced by Wfs1 in the hypothalamus and hippocampus using RNA-sequencing. We used WFS1-deficient mice as a model system to analyze the changes in transcriptional networks. The number of differentially expressed genes between hypothalami of WFS1-deficient (Wfs1KO) and wild-type (WT) mice was 43 and between hippocampi 311 with False Discovery Rate (FDR) <0.05. In hypothalamus of Wfs1KO mice one of the most upregulated genes was Avpr1a whilst Avpr1b was significantly upregulated in hippocampus. Trpm8 was the most upregulated gene in the hippocampus of Wfs1KO mice. The functional analysis revealed significant enrichment of networks and pathways associated with protein synthesis, cell-to-cell signaling and interaction, molecular transport, metabolic disease and nervous system development and function. In conclusion, the transcriptomic profiles of WFS1-deficient hypothalamus and hippocampus do indicate the activation of degenerative molecular pathways causing the clinical occurrences typical to Wolfram syndrome.
2017-12-01 | GSE102623 | GEO
Project description:Goal of the experiment: Analysis of gene expression changes in the cortex, striatum, hippocampus, hypothalamus, Drd2-MSNs and Drd1-MSNs of mice with a postnatal, neuron-specific ablation of GLP or G9a as compared to control mice. For microarray analysis, hippocampus, hypothalamus, cortex and striatum of Camk2a-Cre; GLPfl/fl, Camk2a-Cre; G9afl/fl and age (10-14 week old) and sex matched littermate controls were used for total RNA purification. Four biological replicates were performed for each experiment. Polyribosome associated mRNAs from five, age (10-14 week old) and sex matched Drd1-Cre; Drd1-bacTRAP; G9afl/fl, or Drd2-Cre; Drd2-bacTRAP; G9afl/fl and Drd1-bacTRAP; G9afl/fl or Drd2-bacTRAP; G9afl/fl control mice were used. Three biological replicates were performed for each experiment.
2009-12-10 | E-GEOD-19402 | biostudies-arrayexpress
Project description:Hippocampus and hypothalamus RNA-sequencing of WFS1-deficient mice
| PRJNA398226 | ENA
Project description:Goal of the experiment: Analysis of gene expression changes in the cortex, striatum, hippocampus, hypothalamus, Drd2-MSNs and Drd1-MSNs of mice with a postnatal, neuron-specific ablation of GLP or G9a as compared to control mice.
2009-12-10 | GSE19402 | GEO
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 | PXD002272 | Pride
Project description:Accumulation of negative stressful life events caused major depressive disorder (MDD) a major public health problem related to disability around the world. For effective therapy and disease managements, a comprehensive genomic analysis to identify objective signatures is required to grasp pathophysiological changes and applicable markers. This data was from a chronic mild stress (CMS) induced MDD mouse model followed by Affmatrix cDNA expression array (GeneChip Mouse Genome 430 2.0 Array) analysis in amygdala, hippocampus, prefrontal cortex, and cerebral cortex.
2020-06-05 | GSE151807 | GEO
Project description:Interleukin (IL)-18 is recognized as a multifunctional mediator in inflammation and immune responses. In addition, the production of IL-18 is stimulated by physiological and/or psychological stress implicated in several behavioral disorders. However, it still remains unclear about the role of IL-18 on the central nervous system. In this study, we analyzed gene expression of 6 brain regions; the olfactory bulb, prefrontal cortex, striatum, amygdala, hypothalamus, and hippocampus. Microarray analysis indicated the regional differences of expression in IL-18-/- mice. In particular, the most profound change was observed in the amygdala, in which 1,237 genes were differentially expressed. We purchased IL-18-/- mice and C57BL/6 mice from Charles River Japan . To produce F1 generation mice, three male IL-18-/- mice were mated with six female C57BL/6J mice. We mated F1 mice and created their F2 littermates. Six week-old F2 mice littermates were weaned. At 12 weeks, mice were sacrificed at 14:00 under general anesthesia with diethyl ether. After the systemic perfusion with cold phosphate-buffered saline through the heart using a syringe attached to a 21-G needle, the whole mouse brains were removed. Coronal brain sections (1 mm thick) were prepared on ice using a brain slicer . The olfactory bulb was sliced between 3.5 and 4.5 anterior to bregma. The prefrontal cortex was sliced between 2.5 and 3.5 mm anterior to bregma. The striatum was sliced between -0.5 and 0.5 mm posterior to bregma. The hypothalamus, the amygdala, and the hippocampus were sliced between 1.5 and 2.5 mm posterior to bregma. Total RNA was immediately prepared from these samples using TRIzol and purified by RNeasy kit.
2010-12-01 | E-GEOD-19522 | biostudies-arrayexpress