Glial transcriptome responses to chronic intermittent ethanol exposure
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PROVIDER: PRJNA528097 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: Identify the specific transcriptome alterations in astrocytes and microglia isolated from mouse prefrontal cortex (PFC) following a chronic intermittent ethanol vapor exposure paradigm Methods: We performed RNA-sequencing on astrocytes, microglia, and total homogenate tissue isolated from the PFC of C57BL/6J mice following chronic intermittent ethanol vapor exposure Results: We identified common neuroimmune gene expression response between cell types in response to CIE, unique networks of correlated genes differentially expressed in specific cell types, along with candidate pathways, biological processes and highly connected cell-type specific genes Conclusions: This study sheds light on the cell-specific effects of chronic ethanol and provides novel molecular targets for understanding ethanol dependence
2019-08-20 | GSE128561 | GEO
Project description:Cycles of heavy drinking and abstinence can lead to ethanol abuse disorder. We studied the effects of chronic intermittent ethanol exposure (CIE) over three weeks on neuroblastoma cells, using an ethanol concentration frequently attained in binge drinking (40 mM, 184 mg/dl). There were many changes in gene expression but most were small. CIE affected pathways instrumental in the development or plasticity of neurons, including axonal guidance, reelin signaling and synaptogenesis. Genes involved in dopamine and serotonin signaling were also affected. Changes in transporters and receptors could dampen both NMDA and norepinephrine transmissions. Decreased expression of the GABA transporter SLC6A11 could increase GABA transmission and has been associated with a switch from sweet drinking to ethanol consumption in rats. Ethanol increased stress responses such as unfolded protein response. TGF-β and NFκB signaling were increased. Most of the genes involved in cholesterol biosynthesis were decreased in expression. Withdrawal for 24 h after CIE caused most of the CIE-induced expression changes to move back toward unexposed levels.
2020-09-21 | GSE139408 | GEO
Project description:To understand how chronic intermittent ethanol vapor exposure changes the RNA content of brain-derived extracellular vesicles, we isolated total RNA and used lncRNA/mRNA microarray analysis to examine differential expression following CIE exposure in male animals
2022-01-23 | GSE194160 | GEO
Project description:To understand how chronic intermittent ethanol vapor exposure changes the RNA content of brain-derived extracellular vesicles, we isolated total RNA and used lncRNA/mRNA microarray analysis to examine differential expression following CIE exposure in female animals
2022-01-23 | GSE194159 | GEO
Project description:Effects of chronic intermittent ethanol exposure and withdrawal on neuroblastoma cell transcriptome
| PRJNA579566 | ENA
Project description:We examined global gene expression profiles in amygdala (AMY), nucleus accumbens (NAC), prefrontal cortex (PFC) and Liver of male C57BL/6J mice exposed to 4 cycles of chronic intermittent ethanol (CIE) vapor. Animals were sacrificed at 0, 8, and 120 hr following the last ethanol exposure.
2015-05-26 | GSE60676 | GEO
Project description:Repeated excessive alcohol consumption increases the risk of developing cognitive decline and dementia. Hazardous drinking among older adults further increases such vulnerabilities. In order to understand the molecular mechanisms underlying alcohol-induced cognitive deficits in older adults, we performed a chronic intermittent ethanol exposure paradigm (ethanol or water gavage every other day 10 times) in 8-week-old young adult and 70-week-old aged rats. While spatial memory retrieval ascertained by probe trials in the Morris water maze was not significantly different between ethanol-treated and water-treated rats in both age groups after the fifth and tenth gavages, behavioral flexibility was impaired in ethanol-treated rats than water-treated rats in the aged group but not in the young adult group. Further proteomic and phosphoproteomic analyses on their hippocampal tissues by tandem mass tag mass spectrometry revealed ethanol-treatment-associated proteomic and phosphoproteomic differences distinct to the aged rats, including the upregulations of Prkcd protein level, several of its phosphosites, and its kinase activity and the same aspects in Camk2a but downregulated, and were enriched in pathways involved in neurotransmission regulation, synaptic plasticity, neuronal apoptosis, and insulin receptor signaling. In conclusion, our behavioral and proteomic results added several candidate proteins and pathways potentially associated with alcohol-induced cognitive decline in aged adults.
2023-03-11 | PXD034443 | Pride
Project description:We examined global gene expression profiles in amygdala (AMY), nucleus accumbens (NAC), prefrontal cortex (PFC) and Liver of male C57BL/6J mice exposed to 4 cycles of chronic intermittent ethanol (CIE) vapor. Animals were sacrificed at 0, 8, and 120 hr following the last ethanol exposure. Mice were exposed to 4 cycles of intermittent vapor [4 days of 16 hours vapor/ 8 hours air] with a week between each cycle. Before entry into the vapor chambers, animals were injected with pyrazole (1 mMol/kg) and either ethanol (1.6 g/kg) or saline (controls). Animals were sacrificed at 0, 8, and 120 hr following the last ethanol exposure. The liver 0 hr control group contained 7 animals. Otherwise there were 8 animals per group (treated, control) at each time point.
2015-05-26 | E-GEOD-60676 | biostudies-arrayexpress
Project description:Purpose: Alcohol dependence results in microglia proliferation in brain and changes in microglia morphology and function. However, it remains unknown if microglia initiate or simply amplify the neuroadaptations that lead to alcohol dependence. Here we determined microglia function in chronic intermittent ethanol exposure behaviors using a colony stimulating factor 1 receptor inhibitor (PLX5622) and 3’UTR biased-sequencing. Therefore, the purpose of this study was to provide insight into how microglia may regulate neuroadaptations due to alcohol dependence. Methods: We performed 3’UTR biased transcriptome sequencing (3’Tag-seq) on total homogenate isolated from the prefrontal cortex (PFC) and central nucleus of the amygdala (CeA) of C57BL6/J mice following microglia depletion and chronic intermittent ethanol exposure. Results: Differential expression analysis and WGCNA network analysis revealed that microglia depletion prevents both immune and synaptic gene expression changes that are linked with the formation of alcohol dependence. This suggested that microglia are key regulators of the transition from alcohol misuse to alcohol dependence. Conclusion: Taken together our behavioral and transcriptional data indicate that microglia are the primary effector cell responsible for regulation of alcohol dependence. In addition, our data represents a novel resource for groups interested in transcriptional effects of microglia depletion after alcohol dependence.
2020-11-27 | GSE142571 | GEO
Project description:Despite recent extensive genomic and genetic studies on behavioral responses to ethanol, relatively few new therapeutic targets for the treatment of alcohol use disorder have been validated. Here we describe a cross-species genomic approach focused on identifying gene networks associated with chronic ethanol consumption. To identify brain mechanisms underlying a chronic ethanol consumption phenotype highly relevant to human alcohol use disorder, and to elucidate potential future therapeutic targets, we conducted a genomic study in a nonhuman primate model of chronic open-access ethanol consumption. Microarray analysis of RNA expression in anterior cingulate and subgenual cortices from rhesus macaques was performed across multiple cohorts of animals. Gene networks correlating with ethanol consumption or showing enrichment for ethanol-regulated genes were identified, as were major ethanol-related hub genes within these networks. A subsequent consensus module analysis was used to co-analyze monkey data with expression data from a chronic intermittent ethanol vapor-exposure and consumption model in C57BL/6J mice. Ethanol-related gene networks conserved between primates and rodents were enriched for genes involved discrete biological functions, including; myelination, synaptic transmission, chromatin modification, Golgi apparatus function, translation, cellular respiration, and RNA processing. The myelin-related network, in particular, showed strong correlations with ethanol consumption behavior and displayed marked network reorganization between control and ethanol-drinking animals. Further bioinformatics analysis revealed that these networks also showed highly significant overlap with other ethanol-regulated gene sets. Altogether, these studies provide robust primate and rodent cross-species validation of gene networks associated with chronic ethanol consumption. Our results also suggest potential novel focal points for future therapeutic interventions in alcohol use disorder.
2019-09-03 | GSE134546 | GEO