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Brain expression data from adult mice prenatally exposed to ethanol

ABSTRACT: Moderate alcohol exposure during pregnancy can result in a heterogeneous range of neurobehavioural and cognitive effects, termed fetal alcohol spectrum disorders (FASD). We have developed a mouse model of FASD that involves moderate ethanol exposure throughout gestation achieved by voluntary maternal consumption. This model results in phenotypes relevant to FASD. Since ethanol is known to directly affect the expression of genes in the developing brain leading to abnormal cell death, changes to cell proliferation, migration, and differentiation, and potential changes to epigenetic patterning, we hypothesize that this leaves a long-term footprint on the adult brain. However, the long-term effects of prenatal ethanol exposure on brain gene expression, when behavioural phenotypes are apparent, are unclear. We used a microarray experiment and focused on the genes identified by both to evaluate the genome-wide alterations to the adult brain transcriptome caused by prenatal ethanol exposure. To generate samples, female C57BL/6J mice were given ethanol injections (2.5g/kg of ethanol in saline) twice on gestational days 8 and 11 to produce acute ethanol exposure effects. Control females were injected with the same volume of saline. Females were mated. Whole brain RNA from adult (postnatal day 70) male ethanol-exposed offspring was extracted. RNA samples from three mice were pooled to reduce litter effects and the pooled samples were hybridized on Affymetrix arrays (2 control and 2 ethanol chips, total n=12 mice).

ORGANISM(S): Mus musculus

SUBMITTER: Katarzyna Janus

PROVIDER: E-GEOD-34469 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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brain expression data from adult mice prenatally exposed to ethanol

2011-12-10 | GSE34305 | GEO

Brain expression data from adult mice prenatally exposed to ethanol

Project description:Moderate alcohol exposure during pregnancy can result in a heterogeneous range of neurobehavioural and cognitive effects, termed fetal alcohol spectrum disorders (FASD). We have developed a mouse model of FASD that involves moderate ethanol exposure throughout gestation achieved by voluntary maternal consumption. This model results in phenotypes relevant to FASD. Since ethanol is known to directly affect the expression of genes in the developing brain leading to abnormal cell death, changes to cell proliferation, migration, and differentiation, and potential changes to epigenetic patterning, we hypothesize that this leaves a long-term footprint on the adult brain. However, the long-term effects of prenatal ethanol exposure on brain gene expression, when behavioural phenotypes are apparent, are unclear. We used a microarray experiment and focused on the genes identified by both to evaluate the genome-wide alterations to the adult brain transcriptome caused by prenatal ethanol exposure.

2011-12-16 | GSE34469 | GEO

brain expression data from adult mice prenatally exposed to ethanol

Project description:Moderate alcohol consumption during pregnancy can result in a heterogeneous range of neurobehavioural and cognitive effects, termed fetal alcohol spectrum disorders (FASD). We have developed a mouse moder of FASD that involves moderate ethanol exposure throughout gestation achieved by voluntary maternal consumption. This model results in phenotypes relevant to FASD. Since ethanol is known to directly affect the expression of genes in the developing brain leading to abnormal cell death, changes to cell proliferation, migration, and differentiation, and potential changes to epigenetic patterning, we hypothesize that this leaves a long-term footprint on the adult brain. However, the long-term effects of prenatal ethanol exposure on brain gene expression, when behavioural phenotypes are apparent, are unclear. We used two independent microarray experiments and focused on the genes identified by both to evaluate the genome-wide alterations to the adult brain transcriptome caused by prenatal ethanol exposure via moderate maternal drinking. To generate samples, two independent groups of female C57BL/6J mice were given access to 10% ethanol in water or water only. Control females had access to water only. Females were mated and continued to drink from gestational day 0 to pup postnatal day 10. Whole brain RNA from adult (postnatal day 70) male ethanol-exposed offspring was extracted. For experiment 1, RNA samples from three mice were pooled to reduce litter effects and the pooled samples were hybridized on Affymetrix arrays (2 control and 2 ethanol chips, total n=12 mice). For experiment 2, RNA from two mice were pooled per chip and three arrays per treatment were used (3 control, 3 ethanol, total n=12 mice).

2011-12-10 | E-GEOD-34305 | biostudies-arrayexpress

Brain expression data from fetal mouse brains prenatally exposed to ethanol

Project description:Moderate alcohol exposure during pregnancy can result in brain gene expression changes in resulting offspring. We have developed a mouse model of FASD that involves moderate ethanol exposure in mid-gestation (trimester 2 equivalent) achieved by injections of ethanol. We have previously shown that this model results in phenotypes relevant to FASD. Since ethanol is known to directly affect the expression of genes in the developing brain leading to abnormal cell death, changes to cell proliferation, migration, and differentiation, and potential changes to epigenetic patterning, we hypothesize that there will be gene expression changes immediately following acute ethanol exposure in the fetal brain. We used a microarray experiment and focused on the genes identified to evaluate the genome-wide alterations to the fetal brain transcriptome caused by prenatal ethanol exposure. To generate samples, female C57BL/6J mice were given ethanol injections (2.5g/kg of ethanol in saline) twice on gestational days 14 and 16 to produce acute ethanol exposure effects. Control females were injected with the same volume of saline. Dams were sacrified on gestational day 16, following ethanol exposure, and whole brains from fetuses were then extracted. RNA was isolated from brain tissue and samples from three mice were pooled to reduce litter effects and the pooled samples were hybridized on Affymetrix arrays (2 control and 2 ethanol chips, total n=12 mice).

2013-01-08 | E-GEOD-43324 | biostudies-arrayexpress

Brain expression data from fetal mouse brains prenatally exposed to ethanol

2013-01-08 | GSE43324 | GEO

Modulation of the Drosophila Transcriptome by Developmental Exposure to Alcohol

Project description:Prenatal exposure to ethanol can cause fetal alcohol spectrum disorder (FASD), a prevalent and preventable pediatric disorder. Identifying genetic risk alleles for FASD is impossible in human populations, but the Drosophila genetic model can provide insights. We analyzed changes in genome-wide gene expression in 96 wild-derived inbred fly lines after exposure to alcohol during development. We found extensive sexual dimorphism in the effect of alcohol on gene expression along with effects on adult locomotor activity and sleep. Genetic networks associated with changes in gene expression include both protein-coding and non-coding transcripts, including a female-specific module of small nucleolar RNAs that regulate pseudouridylation of ribosomal RNA. These data support a regulatory role for non-coding elements in response to developmental alcohol exposure.

2022-03-15 | GSE186240 | GEO

Gene expression in the mouse brain following early pregnancy exposure to ethanol [Hippocampus_Males_P21]

Project description:Exposure to alcohol during early embryonic or fetal development has been linked with a variety of adverse outcomes, the most common of which are structural and functional abnormalities of the central nervous system. Behavioral and cognitive deficits reported in individuals exposed to alcohol in utero include intellectual impairment, learning and memory difficulties, diminished executive functioning, attention problems, poor motor function and hyperactivity. The economic and social costs of these outcomes are substantial and profound. Improvement of neurobehavioural outcomes following prenatal alcohol exposure requires greater understanding of the mechanisms of alcohol-induced damage to the brain. Here we use a mouse model of relatively moderate ethanol exposure early in pregnancy and profile gene expression in the hippocampus and caudate putamen of adult male offspring. The effects of offspring sex and age on ethanol-sensitive hippocampal gene expression were also examined.

2016-10-20 | GSE87703 | GEO

Gene expression in the mouse brain following early pregnancy exposure to ethanol [Hippocampus_Females_P87]

2016-10-20 | GSE87700 | GEO

Gene expression in the mouse brain following early pregnancy exposure to ethanol [CaudatePutamen_Males_P87]

2016-10-20 | GSE87699 | GEO

Hippocampal transcriptome analysis following maternal separation in a mouse model of fetal alcohol spectrum disorder

Project description:Fetal alcohol spectrum disorders (FASD) are common, seen in 1-5% of the population in the United States and Canada. Regrettably, children diagnosed with FASD are not likely to remain with their biological parents, facing early maternal separation and foster placements throughout childhood. We have modeled FASD in mice via prenatal alcohol exposure and further induce early life stress through maternal separation. We report an association between adult hippocampal gene expression and prenatal and postnatal treatment that is related to behavioral changes. Clustering of expression profiles through weighted gene co-expression network analysis (WGCNA) identifies a set of transcripts associated with anxiety-like behavior as well as treatment group. Genes in this module are overrepresented by genes involved in transcriptional regulation and other pathways related to neurodevelopment. Interestingly, one member of this module, Polr2a, polymerase (RNA) II (DNA directed) polypeptide A, is downregulated by the combination of prenatal ethanol and postnatal stress in an RNA-Seq experiment and qPCR validation. Together, transcriptional control is implicated as a potential underlying mechanism leading to anxiety-like behavior via environmental insults. Greater understanding of the role of prenatal alcohol exposure and postnatal stress in altering the hippocampal transcriptome in the hippocampus is warranted. Further research is required to elucidate the mechanism involved and use this insight towards early diagnosis and amelioration strategies involving children born with FASD.

2019-06-27 | GSE133369 | GEO

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