Brain expression data from fetal mouse brains prenatally exposed to ethanol
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE43324 | GEO | 2013/01/08
SECONDARY ACCESSION(S): PRJNA185432
REPOSITORIES: GEO
Similar Datasets
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
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.
2011-12-10 | GSE34305 | GEO
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
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. 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).
2011-12-16 | E-GEOD-34469 | biostudies-arrayexpress
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
Project description:The developing brain is particularly sensitive to ethanol during the brain growth spurt or synaptogenesis (third human trimester equivalent). This has been shown to lead to abnormal brain development and behavioural changes in the adult mouse that are relevant to those seen in humans with fetal alcohol spectrum disorders (FASD). We evaluated the long-term (postnatal day 60 young adult) gene expression changes that occur in the brain due to ethanol exposure during synaptogenesis. We used microarray analyses to evaluate the changes in brain gene expression at postnatal day 60 that occur due to ethanol treatment at postnatal days 4 and 7 (synaptogenesis).
2011-12-20 | GSE34549 | GEO
Project description:The developing brain is particularly sensitive to ethanol during the brain growth spurt or synaptogenesis (third human trimester equivalent). This has been shown to lead to abnormal brain development and behavioural changes in the adult mouse that are relevant to those seen in humans with fetal alcohol spectrum disorders (FASD). We evaluated the acute (4h post-treatment) gene expression changes that occur in the brain due to ethanol exposure during synaptogenesis (postnatal day 7). We used microarray analyses to evaluate the changes in brain gene expression at postnatal day 7 that occur due to ethanol treatment at postnatal day 7 (synaptogenesis).
2014-07-18 | GSE59512 | GEO
Project description:Fetal alcohol spectrum disorders (FASD) are a group of neurodevelopmental disorders caused by ethanol exposure in utero, which can result in neurocognitive and behavioral impairments, growth defects, and craniofacial anomalies. FASD affects up to 1-5% of school-aged children in the United States, and there is currently no cure. The underlying mechanisms involved in ethanol teratogenesis remain elusive and need greater understanding to develop and implement effective therapies. Using a third trimester human equivalent postnatal mouse model of FASD, we evaluate the transcriptomic changes induced by ethanol exposure in the cerebellum on P5 and P6, after only 1 or 2 days of ethanol exposure, with the goal of shedding light on the transcriptomic changes induced early during the onset and development of FASD. We have highlighted key pathways and cellular functions altered by ethanol exposure, which include pathways related to immune function and cytokine signaling as well as the cell cycle. Additionally, we found that ethanol exposure resulted in an increase in transcripts associated with a neurodegenerative microglia phenotype, and acute- and pan-injury reactive astrocyte phenotypes. Mixed effects on oligodendrocyte lineage cell associated transcripts and cell cycle associated transcripts were observed. These studies help to elucidate the underlying mechanisms that may be involved with the onset of FASD and provide further insights that may aid in identifying novel targets for interventions and therapeutics.
2023-03-07 | GSE226532 | GEO
Project description:The developing brain is particularly sensitive to ethanol during the brain growth spurt or synaptogenesis (third human trimester equivalent). This has been shown to lead to abnormal brain development and behavioural changes in the adult mouse that are relevant to those seen in humans with fetal alcohol spectrum disorders (FASD). We evaluated the long-term (postnatal day 60 young adult) gene expression changes that occur in the brain due to ethanol exposure during synaptogenesis. We used microarray analyses to evaluate the changes in brain gene expression at postnatal day 60 that occur due to ethanol treatment at postnatal days 4 and 7 (synaptogenesis). To generate samples, C57BL/6J pups were injected with ethanol (experimental) or saline (control) at postnatal days 4 and 7. Pups were weaned at postnatal day 25 and sacrificed at postnatal day 60. Total RNA was extracted from whole brain tissue and RNA from three male mice from three different litters were pooled as one biological replicate. Each male ethanol-treated mouse represented in a sample was matched by a control littermate present in a control sample. This study consists of two biological replicates for each experimental group (total mice used was n=12).
2011-12-20 | E-GEOD-34549 | biostudies-arrayexpress
Project description:The developing brain is particularly sensitive to ethanol during the brain growth spurt or synaptogenesis (third human trimester equivalent). This has been shown to lead to abnormal brain development and behavioural changes in the adult mouse that are relevant to those seen in humans with fetal alcohol spectrum disorders (FASD). We evaluated the acute (4h post-treatment) gene expression changes that occur in the brain due to ethanol exposure during synaptogenesis (postnatal day 7). We used microarray analyses to evaluate the changes in brain gene expression at postnatal day 7 that occur due to ethanol treatment at postnatal day 7 (synaptogenesis). To generate samples, C57BL/6J pups were injected with ethanol (experimental) or saline (control) at postnatal day 7 (2 x 2.5 g/kg at 0h and 2h). Pups were sacrificed 4 hours following the initial injection. Total RNA was extracted from whole brain tissue and RNA from three male mice from three different litters were pooled as one biological replicate. Each male ethanol-treated mouse represented in a sample was matched by a control littermate present in a control sample. This study consists of two experimental (ethanol-treated) biological replicates and four control (saline vehicle-treated) replicates (total mice used was n=18).
2014-07-18 | E-GEOD-59512 | biostudies-arrayexpress