DEG microarray ICR mouse hypothalamus chronic alcohol vs. control_pvalue
Description:
We used a two-bottle free-choice paradigm to measure alcohol drinking [42], and studied effect of chronic alcohol consumption during adolescent development. Male adolescent ICR (outbred) mice (3 weeks of age) were divided into two alcohol groups, one with free access to 5% alcohol, and the other to 10% alcohol, so as to determine if there was a difference in alcohol consumption behavior due to difference in alcohol concentration. In addition, a water-only control group (each mouse had 2 bottles, both filled with water) was used. For brain tissue processing for gene expression analysis, 19 mice with 7 weeks alcohol exposure were selected and grouped into alcohol sample groups (n=1–3 per sample group). Samples A1-A3 had mice with relatively less alcohol consumed (0.50±0.38 g/kg/day); samples A4-A9 had mice with relatively more alcohol consumed (4.80±0.36 g/kg/day); these were significantly different (p<0.05, Unpaired t test with Welch's correction). The rationale for such an approach of sample pooling was to cover the spectrum of mouse alcohol consumption behavior, so that the underlying gene expression patterns may be discernible. For water-only controls, nine mice were selected randomly, and grouped into water sample groups (n=3 per sample group), designated samples C1-C3. RNA samples extracted from hypothalamus were used in gene expression analysis, using the Agilent mouse whole genome microarray chip set.
Authors:
Hong Zou, Ke Wang, Yang Gao, Huaiguang Song, Qinglian Xie, Meilei Jin, Guoping Zhao, Huasheng Xiao, Lei Yu
Whole Brain Gene Expression Correlates for LM_BASELINE measured in BXD RI Males obtained using INIA Brain mRNA M430 (Jun06) RMA. The LM_BASELINE measures Baseline activity in fear conditioning apparatus under the domain Basal Behavior. The correlates were thresholded at a p-value of less than 0.001.
Authors:
Philip VM, Duvvuru S, Gomero B, Ansah TA, Blaha CD, Cook MN, Hamre KM, Lariviere WR, Matthews DB, Mittleman G, Goldowitz D, Chesler EJ
GSE27786_LSK_VS_ERYTHROBLAST_DN
Genes down-regulated in comparison of LSK versus erythroblasts.
c7 - Genesets containing immunologic signatures defined directly from microarray gene expression data from immunologic studies.
Molecular Signatures Database (MSigDB) Geneset. This geneset was imported from one of the MSigDB collections.
gene2msig v. 0.1.0
Last updated 2015.08.31
GSE17721_PAM3CSK4_VS_CPG_12H_BMDM_UP
Genes up-regulated in comparison of dendritic cells (DC) stimulated with Pam3Csk4 (TLR1/2 agonist) at 12 h versus DC cells stimulated with CpG DNA (TLR9 agonist) at 12 h.
c7 - Genesets containing immunologic signatures defined directly from microarray gene expression data from immunologic studies.
Molecular Signatures Database (MSigDB) Geneset. This geneset was imported from one of the MSigDB collections.
gene2msig v. 0.1.0
Last updated 2015.08.31
GSE17721_CPG_VS_GARDIQUIMOD_12H_BMDM_DN
Genes down-regulated in comparison of dendritic cells (DC) stimulated with CpG DNA (TLR9 agonist) at 12 h versus DC cells stimulated with Gardiquimod (TLR7 agonist) at 12 h.
c7 - Genesets containing immunologic signatures defined directly from microarray gene expression data from immunologic studies.
Molecular Signatures Database (MSigDB) Geneset. This geneset was imported from one of the MSigDB collections.
gene2msig v. 0.1.0
Last updated 2015.08.31
GSE27786_LIN_NEG_VS_ERYTHROBLAST_DN
Genes down-regulated in comparison of lineage negative versus erythroblasts.
c7 - Genesets containing immunologic signatures defined directly from microarray gene expression data from immunologic studies.
Molecular Signatures Database (MSigDB) Geneset. This geneset was imported from one of the MSigDB collections.
gene2msig v. 0.1.0
Last updated 2015.08.31
GSE32423_CTRL_VS_IL7_MEMORY_CD8_TCELL_UP
Genes up-regulated in comparison of memory CD8 T cells versus those treated with IL7 <a href='http://www.ncbi.nlm.nih.gov/gene/3574'>[GeneID=3574]</a>.
c7 - Genesets containing immunologic signatures defined directly from microarray gene expression data from immunologic studies.
Molecular Signatures Database (MSigDB) Geneset. This geneset was imported from one of the MSigDB collections.
gene2msig v. 0.1.0
Last updated 2015.08.31
Differential gene expression in nucleus accumbens somatostatin interneurons_cocaine_mice_pvalue
Description:
To characterize transcriptional alterations that cocaine induces in these cells, we perform cell type-specific RNA-sequencing on FACS-isolated nuclei of somatostatin interneurons and identified 1100 DETs enriched for processes related to neural plasticity. To profile the entire (non poly-A selected) transcriptome of NAc somatostatin interneurons, we generated a transgenic reporter line (SST-TLG498 mice) to label the nuclei of these cells with a modified form of EGFP that is retained in the nuclear membrane (EGFP-F)22, enabling their isolation from NAc dissections using FACS. We succeeded in FACS-isolating nuclei suitable for RNA-sequencing from individual SST-TLG498 mice. We proceeded with differential expression analysis of the RNA-sequencing data to identify differentially expressed transcripts (DETs) in NAc somatostatin interneurons in response to repeated cocaine exposure: 778 transcripts were upregulated by cocaine and 322 were downregulated.
Authors:
Efrain A Ribeiro, Marine Salery, Joseph R Scarpa, Erin S Calipari, Peter J Hamilton, Stacy M Ku, Hope Kronman, Immanuel Purushothaman, Barbara Juarez, Mitra Heshmati, Marie Doyle, Casey Lardner, Dominicka Burek, Ana Strat, Stephen Pirpinias, Ezekiell Mouzon, Ming-Hu Han, Rachael L Neve, Rosemary C Bagot, Andrew Kasarskis, Ja Wook Koo, Eric J Nestler
Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that act as ligand-activated transcription factors. Although prescribed for dyslipidemia and type-II diabetes, PPAR agonists also possess anti-addictive characteristics. PPAR agonists decrease ethanol consumption and reduce withdrawal severity and susceptibility to stress-induced relapse in rodents. However, the cellular and molecular mechanisms facilitating these properties have yet to be investigated. We tested three PPAR agonists in a continuous access two-bottle choice (2BC) drinking paradigm and found that tesaglitazar (PPARα/γ; 1.5 mg/kg) and fenofibrate (PPARα; 150 mg/kg) decreased ethanol consumption in male C57BL/6J mice while bezafibrate (PPARα/γ/β; 75 mg/kg) did not. We hypothesized that changes in brain gene expression following fenofibrate and tesaglitazar treatment lead to reduced ethanol drinking. We studied unbiased genomic profiles in areas of the brain known to be important for ethanol dependence, the prefrontal cortex (PFC) and amygdala, and also profiled gene expression in liver. Genomic profiles from the non-effective bezafibrate treatment were used to filter out genes not associated with ethanol consumption. Because PPAR agonists are anti-inflammatory, they would be expected to target microglia and astrocytes. Surprisingly, PPAR agonists produced a strong neuronal signature in mouse brain, and fenofibrate and tesaglitazar (but not bezafibrate) targeted a subset of GABAergic interneurons in the amygdala. Weighted gene co-expression network analysis (WGCNA) revealed co-expression of treatment-significant genes. Functional annotation of these gene networks suggested that PPAR agonists might act via neuropeptide and dopaminergic signaling pathways in the amygdala. Our results reveal gene targets through which PPAR agonists can affect alcohol consumption behavior.
Authors:
Laura B Ferguson, Dana Most, Yuri A Blednov, R Adron Harris
Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that act as ligand-activated transcription factors. Although prescribed for dyslipidemia and type-II diabetes, PPAR agonists also possess anti-addictive characteristics. PPAR agonists decrease ethanol consumption and reduce withdrawal severity and susceptibility to stress-induced relapse in rodents. However, the cellular and molecular mechanisms facilitating these properties have yet to be investigated. We tested three PPAR agonists in a continuous access two-bottle choice (2BC) drinking paradigm and found that tesaglitazar (PPARα/γ; 1.5 mg/kg) and fenofibrate (PPARα; 150 mg/kg) decreased ethanol consumption in male C57BL/6J mice while bezafibrate (PPARα/γ/β; 75 mg/kg) did not. We hypothesized that changes in brain gene expression following fenofibrate and tesaglitazar treatment lead to reduced ethanol drinking. We studied unbiased genomic profiles in areas of the brain known to be important for ethanol dependence, the prefrontal cortex (PFC) and amygdala, and also profiled gene expression in liver. Genomic profiles from the non-effective bezafibrate treatment were used to filter out genes not associated with ethanol consumption. Because PPAR agonists are anti-inflammatory, they would be expected to target microglia and astrocytes. Surprisingly, PPAR agonists produced a strong neuronal signature in mouse brain, and fenofibrate and tesaglitazar (but not bezafibrate) targeted a subset of GABAergic interneurons in the amygdala. Weighted gene co-expression network analysis (WGCNA) revealed co-expression of treatment-significant genes. Functional annotation of these gene networks suggested that PPAR agonists might act via neuropeptide and dopaminergic signaling pathways in the amygdala. Our results reveal gene targets through which PPAR agonists can affect alcohol consumption behavior.
Authors:
Laura B Ferguson, Dana Most, Yuri A Blednov, R Adron Harris
Genes with particular expression in the Anterior olfactory nucleus, dorsal part. Data represent fold expression difference in structure versus grey matter average expression.
Genes with particular expression in the Orbital area, lateral part, layer 1. Data represent fold expression difference in structure versus grey matter average expression.
Genes with particular expression in the Orbital area, ventrolateral part, layer 1. Data represent fold expression difference in structure versus grey matter average expression.
Genes with particular expression in the Granular lamina of the cochlear nuclei. Data represent fold expression difference in structure versus grey matter average expression.
Genes with particular expression in the Koelliker-Fuse subnucleus. Data represent fold expression difference in structure versus grey matter average expression.
Genes with particular expression in the Anterior olfactory nucleus, external part. Data represent fold expression difference in structure versus grey matter average expression.
Genes with particular expression in the Anterior olfactory nucleus, lateral part. Data represent fold expression difference in structure versus grey matter average expression.
Genes with particular expression in the Parabigeminal nucleus. Data represent fold expression difference in structure versus grey matter average expression.
QTL associated with loss of righting induced by ethanol 8. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (154849280)
Authors:
Radcliffe RA, Bohl ML, Lowe MV, Cycowski CS, Wehner JM
Add Selected GeneSets to Project(s)
Warning: You are not signed in. Adding these genesets to a project will create a guest account for you.
Guest accounts are temporary, and will be removed within 24 hours of creation. Guest accounts can be registered as full accounts, but you cannot associate a guest account with an existing account.
If you already have an account, you should sign into that account before proceeding.