Warning: You're using a guest account.
Unless you register as a full user all information associated with this session will be deleted within 24 hours.
Ethanol Induced Hypothermia Chr# 16 rs4182243(46052770) with right flanking marker rs4165065(17412172) and left marker rs4200124(70695141). This was mapped in 300 + (b6x129)F2 mice.
Kyoto Encyclopedia of Genes and Genomes (KEGG) Geneset. This geneset contains genes that participate in the "Oxidative phosphorylation" pathway. This set was automatically constructed using the KEGG API and enumerating all mouse pathways.
gene2kegg v. 0.1.1
Last updated 2015.09.10
Kyoto Encyclopedia of Genes and Genomes (KEGG) Geneset. This geneset contains genes that participate in the "Huntington's disease" pathway. This set was automatically constructed using the KEGG API and enumerating all mouse pathways.
gene2kegg v. 0.1.1
Last updated 2015.09.10
Kyoto Encyclopedia of Genes and Genomes (KEGG) Geneset. This geneset contains genes that participate in the "Parkinson's disease" pathway. This set was automatically constructed using the KEGG API and enumerating all mouse pathways.
gene2kegg v. 0.1.1
Last updated 2015.09.10
Kyoto Encyclopedia of Genes and Genomes (KEGG) Geneset. This geneset contains genes that participate in the "Alzheimer's disease" pathway. This set was automatically constructed using the KEGG API and enumerating all mouse pathways.
gene2kegg v. 0.1.1
Last updated 2015.09.10
Kyoto Encyclopedia of Genes and Genomes (KEGG) Geneset. This geneset contains genes that participate in the "Non-alcoholic fatty liver disease (NAFLD)" pathway. This set was automatically constructed using the KEGG API and enumerating all mouse pathways.
gene2kegg v. 0.1.1
Last updated 2015.09.10
Kyoto Encyclopedia of Genes and Genomes (KEGG) Geneset. This geneset contains genes that participate in the "Metabolic pathways" pathway. This set was automatically constructed using the KEGG API and enumerating all mouse pathways.
gene2kegg v. 0.1.1
Last updated 2015.09.10
Genes associated with Mus musculus that interact with the MeSH term 'Nanotubes, Carbon' (D037742). Incorporates data from 26 publications curated by the Comparative Toxicogenomics Database (CTD). ODE Gene scores represent number of supporting publications per gene.
Genes associated with Mus musculus that interact with the MeSH term 'Chlorodiphenyl (54% Chlorine)' (D020111). Incorporates data from 317 publications curated by the Comparative Toxicogenomics Database (CTD). ODE Gene scores represent number of supporting publications per gene.
Genes associated with Mus musculus that interact with the MeSH term 'Tetrachlorodibenzodioxin' (D013749). Incorporates data from 2 publications curated by the Comparative Toxicogenomics Database (CTD). ODE Gene scores represent number of supporting publications per gene.
Genes associated with Mus musculus that interact with the MeSH term 'Tetracaine' (D013748). Incorporates data from 12365 publications curated by the Comparative Toxicogenomics Database (CTD). ODE Gene scores represent number of supporting publications per gene.
Genes associated with Mus musculus that interact with the MeSH term 'Clofibrate' (D002994). Incorporates data from 18 publications curated by the Comparative Toxicogenomics Database (CTD). ODE Gene scores represent number of supporting publications per gene.
Genes associated with Mus musculus that interact with the MeSH term 'rosiglitazone' (C089730). Incorporates data from 116 publications curated by the Comparative Toxicogenomics Database (CTD). ODE Gene scores represent number of supporting publications per gene.
Genes associated with Mus musculus that interact with the MeSH term 'pirinixic acid' (C006253). Incorporates data from 1 publications curated by the Comparative Toxicogenomics Database (CTD). ODE Gene scores represent number of supporting publications per gene.
Genes associated with Mus musculus that interact with the MeSH term 'sinefungin' (C006235). Incorporates data from 6366 publications curated by the Comparative Toxicogenomics Database (CTD). ODE Gene scores represent number of supporting publications per gene.
Microglia depletion and alcohol gene expression logFC
Description:
Alcohol abuse induces changes in microglia morphology and immune function, but whether microglia initiate or simply amplify the harmful effects of alcohol exposure is still a matter of debate. Here, we determine microglia function in acute and voluntary drinking behaviors using a colony-stimulating factor 1 receptor inhibitor (PLX5622). We show that microglia depletion does not alter the sedative or hypnotic effects of acute intoxication. Microglia depletion also does not change the escalation or maintenance of chronic voluntary alcohol consumption. Transcriptomic analysis revealed that although many immune genes have been implicated in alcohol abuse, down regulation of microglia genes does not necessitate changes in alcohol intake. Instead, microglia depletion and chronic alcohol result in compensatory upregulation of alcohol-responsive, reactive astrocyte genes, indicating astrocytes may play a role in regulation of these alcohol behaviors. Taken together, our behavioral and transcriptional data indicate that microglia are not theprimary effector cell responsible for regulation of acute and voluntary alcohol behaviors. Because microglia depletion did not regulate acute or voluntary alcohol behaviors, we hypothesized that these doses were insufficient to activate microglia and recruit them to an effector phenotype. Therefore, we used a model of repeated immune activation using polyinosinic:polycytidylic acid
Microglia depletion and alcohol gene expression p-value
Description:
Alcohol abuse induces changes in microglia morphology and immune function, but whether microglia initiate or simply amplify the harmful effects of alcohol exposure is still a matter of debate. Here, we determine microglia function in acute and voluntary drinking behaviors using a colony-stimulating factor 1 receptor inhibitor (PLX5622). We show that microglia depletion does not alter the sedative or hypnotic effects of acute intoxication. Microglia depletion also does not change the escalation or maintenance of chronic voluntary alcohol consumption. Transcriptomic analysis revealed that although many immune genes have been implicated in alcohol abuse, down regulation of microglia genes does not necessitate changes in alcohol intake. Instead, microglia depletion and chronic alcohol result in compensatory upregulation of alcohol-responsive, reactive astrocyte genes, indicating astrocytes may play a role in regulation of these alcohol behaviors. Taken together, our behavioral and transcriptional data indicate that microglia are not theprimary effector cell responsible for regulation of acute and voluntary alcohol behaviors. Because microglia depletion did not regulate acute or voluntary alcohol behaviors, we hypothesized that these doses were insufficient to activate microglia and recruit them to an effector phenotype. Therefore, we used a model of repeated immune activation using polyinosinic:polycytidylic acid
We investigated the role of microglia in a mouse model of alcohol dependence using a colony stimulating factor 1 receptor inhibitor (PLX5622) to deplete microglia and a chronic intermittent ethanol vapor two-bottle choice drinking procedure. Additionally, we examined anxiety-like behavior during withdrawal. We then analyzed synaptic neuroadaptations in the central nucleus of the amygdala (CeA) and gene expression changes in the medial prefrontal cortex (mPFC) and CeA from the same animals used for behavioral studies.
Alcohol dependence in the medial prefrontal cortex q-value
Description:
We investigated the role of microglia in a mouse model of alcohol dependence using a colony stimulating factor 1 receptor inhibitor (PLX5622) to deplete microglia and a chronic intermittent ethanol vapor two-bottle choice drinking procedure. Additionally, we examined anxiety-like behavior during withdrawal. We then analyzed synaptic neuroadaptations in the central nucleus of the amygdala (CeA) and gene expression changes in the medial prefrontal cortex (mPFC) and CeA from the same animals used for behavioral studies.
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
GeneWeaver