Mouse cerebellar libraries:Ethanol-treated and controls
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE4520 | GEO | 2006/11/22
SECONDARY ACCESSION(S): PRJNA94605
REPOSITORIES: GEO
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Project description:P300 and P720 C57BL6/J male mice were exposed to ethanol vapor (95% w/v) for 3 hours each day for a total of 5 days. Blood alcohol levels in the ethanol treated animals was 3.0mg/ml. Controls at P300 and P720 were included. Keywords: SAGE-dose response All C57BL/6 male mice were sacrificed and the cerebellum was quickly removed. Total RNA was isolated using Trizol. For the creation of the libraries, 40micrograms of total RNA was used. cDNA was synthesized on oligo dt beads. Enzyme: NlaIII Vector: pZERO-I
2006-11-21 | E-GEOD-4520 | biostudies-arrayexpress
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2006-10-31 | GSE5186 | GEO
Project description:To better understand the molecular mechanisms underlying ethanol action we have developed an assay system to study sensitivity and fast and chronic tolerance to the sedative effects of ethanol. Flies developed fast ethanol tolerance after single exposure to 50% of ethanol vapor for 40 min. Flies can also develope chronic ethanol tolerance after 5x 40 min exposure to 50% ethanol vapor interspersed with 4x 80 min exposure to 10% ethanol vapor. We used microarray analysis to identify genes involved in the development of fast and chronic ethanol tolerance in Drosophila. More than 600 hundred genes were found to have changed their expression level in response to different ethanol treatment. Among these genes, Homer was picked for further study and is demonstrated that its expression in ellipsoid body is critical for the normal sensitivity and fast toleance to ethanol. Keywords: time course
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Project description:To better understand the molecular mechanisms underlying ethanol action we have developed an assay system to study sensitivity and fast and chronic tolerance to the sedative effects of ethanol. Flies developed fast ethanol tolerance after single exposure to 50% of ethanol vapor for 40 min. Flies can also develope chronic ethanol tolerance after 5x 40 min exposure to 50% ethanol vapor interspersed with 4x 80 min exposure to 10% ethanol vapor. We used microarray analysis to identify genes involved in the development of fast and chronic ethanol tolerance in Drosophila. More than 600 hundred genes were found to have changed their expression level in response to different ethanol treatment. Among these genes, Homer was picked for further study and is demonstrated that its expression in ellipsoid body is critical for the normal sensitivity and fast toleance to ethanol. Keywords: time course Whole heads of 3 groups of Drosophila were separated for RNA extraction and hybridization on Affymetrix microarrays. These 3 groups of flies were treated with different ethanol treatment. Naive group of flies (GSM101531, GSM101532, GSM101533, GSM101534, GSM101535, GSM101536) received only 50 min of humidified air. Fast group of flies (GSM101537, GSM101538, GSM101539, GSM101540, GSM101541, GSM101542) received humidified air for 50 min followed by a single exposure of 50% ethanol vapor for 40 min. Chronic group of flies (GSM101543, GSM101544, GSM101545, GSM101546, GSM101547, GSM101548) ) received humidified air for 50 min followed by 5 exposures of 50% ethanol vapor for 40 min.
2006-03-24 | E-GEOD-4531 | biostudies-arrayexpress
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
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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.
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Project description:Rats were trained to orally self-administer alcohol in a concurrent, two-lever, free-choice contingency using a modification of the sweet solution fading procedure (O'Dell et al., 2004; Roberts et al., 2000; Vendruscolo et al., 2012). Following acquisition of self-administration, rats were allowed to self-administer unsweetened alcohol (10%) for 4 weeks and were then assigned to two groups matched by levels of responding: one group (dependent group) was exposed to chronic, intermittent ethanol vapors for 4 weeks to induce dependence; the other group (nondependent group) was not exposed to ethanol vapor. After a month of vapor exposure, rats were again tested during acute withdrawal (6-8 hours after removal from the vapor chambers) until stable levels of alcohol intake were achieved. As expected, alcohol vapor-exposed rats self-administered significantly greater amounts of alcohol than control rats not exposed to alcohol vapor during acute withdrawal. Rats were sacrificed during protracted abstinence (3 weeks after the end of alcohol vapor exposure) along with age-matched alcohol naive rats. 96 gene expression profiles (GEP) were obtained from 8 brain regions believed to be relevant in alcoholM-bM-^@M-^Ys reinforcing properties using the Affymetrix RN230.2 platform. Specifically, the following brain regions were microdissected and analyzed from nondependent and dependent alcohol self-administering rats as well as age-matched alcohol naive rats: (a) medial prefrontal cortex (MPF), (b) shell and (c) core NAc sub-regions, (d) central nucleus (CeA) and (e) basolateral nucleus of the amygdala (BLA), (f) dorsolateral and (g) ventral bed nucleus of the stria terminalis (BNST), and (h) ventral tegmental area (VTA).
2014-11-13 | E-GEOD-60966 | biostudies-arrayexpress
Project description:Purpose: Fetal alcohol spectrum disorders (FASD) result from ethanol exposure to the developing fetus. FASD occur in up to 1-5% of live births in the United States and there currently is no cure. Ethanol exposure to the developing central nervous system (CNS) has profound effects on learning and memory, impulse control, and motor function, resulting from neuropathology. The purpose of the current study was to perform transcriptome analysis to evaluate the effects of early postnatal ethanol exposure in the hippocampus and cerebellum. Methods: Postnatal C57BL/6 mice were treated with 4g/kg of ethanol from P4-P9, brains were harvested 24h after the final treatment at P10, hippocampi and cerebella were microdissected, RNA was isolated, and RNASeq analysis was performed. We compared differences in gene expression, sex-dependent expression, and global biological pathways associated with disruptions in hippocampal and cerebellar genes between the ethanol and vehicle treated neonates. Results: Ethanol caused both an up and down regulation of genes associated with the hippocampus and cerebellum, which may result in the disruption of normal circuitry and maturation and growth in these brain regions. Ethanol increased the expression of genes associated with the S phase of the cell cycle in both the hippocampus and cerebellum. In the cerebellum, ethanol increased effector gene expression, and in the hippocampus, genes associated with different interneuron lineages were altered. Postnatal ethanol exposure also resulted in altered expression of genes associated with oligodendrocyte lineages and myelination, along with alterations in microglia associated genes. Conclusion: Collectively, these data indicate that ethanol has profound effects on the hippocampus and cerebellum, resulting in alterations of gene expression and biological pathways regulating neurodevelopment. These studies may have important implications concerning alcohol-induced neuropathology and the neurological effects seen across the life span in FASD.
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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