Cerebellar Gene Expression Profile Analysis in a Rat Model of Acute Alcohol Intoxication
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE49303 | GEO | 2013/07/29
SECONDARY ACCESSION(S): PRJNA213605
REPOSITORIES: GEO
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Project description:To identify possible target molecules for acute alcohol intoxication therapy, we used microarray analysis to compare cerebella gene expression profiles of control and acute alcohol-intoxicated rats. We first established a model of acute alcohol intoxication in SD rats, and then used rat cDNA microarray to profile mRNA expression in the cerebella of alcohol-intoxicated rats (experimental group) and saline-treated rats (control group). A six chip study using total RNA recovered from three separate experimental groups and three separate control groups. We first established a model of acute alcohol intoxication in SD rats, and then used rat cDNA microarray to profile mRNA expression in the cerebella of alcohol-intoxicated rats (experimental group) and saline-treated rats (control group). Cerebellar tissues from three rats were ground to a mixed sample,so we use 3 rats in one group.
2013-07-29 | E-GEOD-49303 | biostudies-arrayexpress
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.
2014-11-13 | GSE60966 | GEO
Project description:The impact of alcohol abuse on AD is poorly understood. Here we show that the onset of neurocognitive impairment in a mouse model of AD is hastened by repeated alcohol intoxication through exposure to alcohol vapor and we provide a comprehensive gene expression dataset of the prefrontal cortex by single nucleus RNA sequencing of 113,242 cells. Several genes previously associated with AD in humans by GWAS were differentially regulated in specific neuronal populations. Gene expression patterns of AD mice with a history of alcohol intoxication were more similar to the gene expression signatures of older AD mice with more advanced disease and cognitive impairment than to those of younger AD mice with prodromic disease, suggesting that alcohol promotes transcriptional changes consistent with AD progression. Our gene expression dataset at the single cell level provides a unique resource for investigations of the molecular bases of the detrimental role of excessive alcohol intake in AD.
2023-06-09 | GSE218309 | GEO
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:Here, we examined the effects of alcohol on global gene expression in the CeA using a chronic intermittent ethanol (CIE) vapor model in rats and RNA sequencing (RNA-Seq). The CIE procedure resulted in robust changes in CeA gene expression during intoxication; as the number of differentially expressed genes (DEGs) was significantly greater than those expected by chance. Over-representation analysis of cell types; functional groups and molecular pathways revealed biological categories potentially important for the development of alcohol dependence in our model.
2020-10-07 | GSE159136 | GEO
Project description:Adolescent binge alcohol exposure has been previously shown to have long-lasting effects on the expression of hypothalamic genes that regulate the stress response, even in the absence of subsequent adult alcohol exposure. Those data suggested that alcohol can induce permanent gene expression changes, potentially through epigenetic modifications. Importantly, epigenetic modifications can be transmitted to future generations therefore, in these studies we investigated the effects of adolescent binge alcohol exposure on hypothalamic gene expression patterns in the F1 generation offspring. It has been well documented that maternal alcohol exposure during fetal development can have devastating neurological consequences. However, less is known about the consequences of maternal and/or paternal alcohol exposure outside of the gestational time frame. Here, we exposed adolescent male and female rats to a repeated binge EtOH exposure paradigm and then mated them in adulthood. Hypothalamic samples were taken from the offspring of these animals at postnatal day (PND) 7 and subjected to a genome-wide microarray analysis followed by qRT-PCR for selected genes. Importantly, the parents were not intoxicated at the time of mating and were not exposed to EtOH at any time during gestation therefore, the offspring were never directly exposed to EtOH. Our results showed that the offspring of alcohol-exposed parents had significant differences in the expression of hypothalamic genes that mediate neurogenesis and synaptic plasticity during neurodevelopment, genes important for directing chromatin remodeling, posttranslational modifications or transcription regulation, as well as genes involved in regulation of obesity and reproductive function. These data demonstrate that repeated binge alcohol exposure during pubertal development can potentially have detrimental effects on future offspring even in the absence of direct fetal alcohol exposure.
2014-03-19 | GSE53028 | GEO
Project description:Circadian rhythms are central to optimal physiological functioning and their interruption contributes to the development of several chronic diseases. Alcohol (EtOH) intoxication disrupts circadian rhythms within liver, brain, and intestines, but it is unknown whether alcohol also disrupts components of the core clock in skeletal muscle. Female C57BL/6Hsd mice were randomized to receive either saline (control) or alcohol (EtOH) (5g/kg) via intraperitoneal injection at the start of the dark cycle (ZT12), and gastrocnemius was collected every 4hr from Control and EtOH treated mice for the next 48hr following isoflurane anesthetization. In addition, metyrapone was administered prior to alcohol intoxication in separate mice to determine whether the alcohol-induced increase in serum corticosterone contributed to circadian gene regulation. Finally, synchronized C2C12 myotubes were treated with alcohol (100mM) to assess the influence of centrally or peripherally mediated effects of alcohol on the muscle clock. Alcohol significantly disrupted the mRNA expression of Bmal1, Per1/2, and Cry1/2 in addition to perturbing the clock-controlled genes, Myod1, Dbp, Tef, and Bhlhe40 (p<0.05). Alcohol increased serum corticosterone levels and glucocorticoid target genes, Redd1 and Klf15, in muscle. Metyrapone decreased serum corticosterone in EtOH mice but did not normalize the mRNA expression of Per1, Cry1 and Cry2 and Myod1 which were altered by EtOH. Alcohol did not alter core clock gene expression (Bmal, Per1/2, Cry1/2) at 4, 8, and 12hrs post treatment in synchronized C2C12 myotubes. Therefore, binge alcohol disrupted genes of the core molecular clock independently of elevated serum corticosterone.
2021-09-10 | GSE183665 | GEO
Project description:The objective of this study was to determine changes in gene expression within the extended amygdala following binge-like alcohol drinking by adolescent alcohol-preferring (P) rats. Starting at 28 days of age, P rats were given concurrent access to 15 and 30 % ethanol for 3 one-h sessions for 5 consecutive days each week until they were 49 days old. Rats were killed by decapitation 3 h after the first ethanol access session on the 15th day of drinking. RNA was prepared from micropunch samples of the nucleus accumbens shell (Acb-sh) and central nucleus of the amygdala (CeA). Ethanol intakes were 2.5 – 3.0 g/kg/session. There were 154 and 182 unique named genes that significantly differed (FDR = 0.2) between the water and ethanol group in the Acb-sh and CeA, respectively. Gene Ontology (GO) analyses indicated that adolescent binge drinking produced changes in the in biological processes involved in cell proliferation and regulation of cellular structure in the Acb-sh, and in neuron projection and positive regulation of cellular organization in the CeA. Ingenuity Pathway Analysis indicated that, in the Acb-sh, there were several major intracellular signaling pathways (e.g., cAMP-mediated and protein kinase A signaling pathways) altered by adolescent drinking, with 3-fold more genes up-regulated than down-regulated in the alcohol group. The cAMP-mediated signaling system was also up-regulated in the CeA of the alcohol group. Weighted gene co-expression network analysis (WGCNA) indicated significant G-protein coupled receptor signaling and transmembrane receptor protein kinase signaling categories in the Acb-sh and CeA, respectively. Overall, the results of this study indicated that binge-like alcohol drinking by adolescent P rats is differentially altering the expression of genes in the Acb-sh and CeA, some of which are involved in intracellular signaling pathways and may produce long-term changes in neuronal function.
2013-07-20 | GSE49041 | GEO
Project description:The objective of this study was to determine changes in gene expression within the extended amygdala following binge-like alcohol drinking by adolescent alcohol-preferring (P) rats. Starting at 28 days of age, P rats were given concurrent access to 15 and 30 % ethanol for 3 one-h sessions for 5 consecutive days each week until they were 49 days old. Rats were killed by decapitation 3 h after the first ethanol access session on the 15th day of drinking. RNA was prepared from micropunch samples of the nucleus accumbens shell (Acb-sh) and central nucleus of the amygdala (CeA). Ethanol intakes were 2.5 – 3.0 g/kg/session. There were 154 and 182 unique named genes that significantly differed (FDR = 0.2) between the water and ethanol group in the Acb-sh and CeA, respectively. Gene Ontology (GO) analyses indicated that adolescent binge drinking produced changes in the in biological processes involved in cell proliferation and regulation of cellular structure in the Acb-sh, and in neuron projection and positive regulation of cellular organization in the CeA. Ingenuity Pathway Analysis indicated that, in the Acb-sh, there were several major intracellular signaling pathways (e.g., cAMP-mediated and protein kinase A signaling pathways) altered by adolescent drinking, with 3-fold more genes up-regulated than down-regulated in the alcohol group. The cAMP-mediated signaling system was also up-regulated in the CeA of the alcohol group. Weighted gene co-expression network analysis (WGCNA) indicated significant G-protein coupled receptor signaling and transmembrane receptor protein kinase signaling categories in the Acb-sh and CeA, respectively. Overall, the results of this study indicated that binge-like alcohol drinking by adolescent P rats is differentially altering the expression of genes in the Acb-sh and CeA, some of which are involved in intracellular signaling pathways and may produce long-term changes in neuronal function.
2013-07-20 | GSE49040 | GEO
Project description:Gene expression was analyzed in brains of 4 male selectively-bred alcohol-preferring (P) rats (generation 63) and 3 male alcohol non-preferring (NP) rats (generation 62) that were obtained from Dr. Richard L. Bell, Indiana University School of Medicine, Indianapolis, IN. These rats had never been exposed to alcohol. Individual rats from each group were hybridized separately to individual arrays (one array per rat). No duplicates are present. Originally, four NP samples were analyzed, but one was dropped because of quality control standards.
2011-04-19 | E-GEOD-15764 | biostudies-arrayexpress