Ontology highlight
ABSTRACT:
PROVIDER: PRJNA259765 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1561060.fastq.gz | Fastqsanger.gz | |||
| SRR1561070.fastq.gz | Fastqsanger.gz | |||
| SRR1561080.fastq.gz | Fastqsanger.gz | |||
| SRR1561090.fastq.gz | Fastqsanger.gz | |||
| SRR1561100.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Effects of acute prenatal exposure to ethanol on microRNA expression are ameliorated by environmental manipulation.
| PRJNA259613 | ENA
Project description:Effects of acute prenatal exposure to ethanol on microRNA expression are ameliorated by environmental manipulation
| PRJNA259768 | ENA
Project description:Maternal alcohol consumption during pregnancy results in a spectrum of lifelong behavioral and cognitive deficits collectively known as Fetal Alcohol Spectrum Disorders (FASD). FASD is a major health burden in most societies, there is no cure, and the molecular mechanism involved in its development is poorly understood. Human neurodevelopment is a continuum that extends over two decades after birth, with the potential to influence outcomes both prenatally and postnatally. Here, we experimentally investigate if positive postnatal environment enrichment ameliorates behavioral deficits caused by ethanol exposure. Furthermore, we assessed if this modulation is associated with alterations in hippocampal gene expression. To accomplish this, we used a binge model of ethanol exposure followed by environmental enrichment in C57BL/6 mice to generate four groups of animals: (1) control mice raised in standard conditions, (2) mice raised in enriched environments, (3) ethanol-exposed mice raised in standard conditions, and (4) ethanol-exposed mice raised in enriched environments. The environmental enrichment includes larger home cages with more individuals for social interaction, regular exposure to novel items, and access to running wheels. Ethanol exposure results in anxiety-like behavior (light-dark box) as well as learning and memory deficits (Barnes maze) that are at least partially ameliorated by enrichment. Environmental enrichment also improves performance for individuals not exposed to ethanol. Ethanol exposure induces changes in adult hippocampal gene expression (RNA-Seq). Some of the changes in adult hippocampal gene expression following ethanol exposure are reversed by environmental enrichment. The results offer a potential mechanism of behavioral deficits caused by ethanol exposure, including the potential for amelioration after an FASD diagnosis.
2021-09-24 | GSE184615 | GEO
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
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:In this study, we tested if miRNAs are altered in amygdala and ventral striatum as a consequence of prenatal ethanol exposure and/or social enrichment. miRNA samples from 72 male and female adolescent rats were analyzed by RNA-Seq analysis and Affymetrix miRNA arrays. Several miRNAs showed significant changes due to prenatal ethanol exposure or social enrichment in one or both brain regions. Some of the miRNA changes caused by ethanol were reversed by social enrichment. The top predicted gene targets of these miRNAs were mapped and subjected to pathway enrichment analysis. We also directly examined the evidence for modulation of target mRNAs in whole transcriptome microarray data from the same rats. Among the pathways most strongly affected were p53, CREB, Glutamate and GABA signaling. Together, our data suggest a number of novel epigenetic mechanisms for social enrichment to reverse the effects of ethanol exposure.
2014-08-28 | GSE60819 | GEO
Project description:In this study, we tested if miRNAs are altered in amygdala and ventral striatum as a consequence of prenatal ethanol exposure and/or social enrichment. miRNA samples from 72 male and female adolescent rats were analyzed by RNA-Seq analysis and Affymetrix miRNA arrays. Several miRNAs showed significant changes due to prenatal ethanol exposure or social enrichment in one or both brain regions. Some of the miRNA changes caused by ethanol were reversed by social enrichment. The top predicted gene targets of these miRNAs were mapped and subjected to pathway enrichment analysis. We also directly examined the evidence for modulation of target mRNAs in whole transcriptome microarray data from the same rats. Among the pathways most strongly affected were p53, CREB, Glutamate and GABA signaling. Together, our data suggest a number of novel epigenetic mechanisms for social enrichment to reverse the effects of ethanol exposure.
2014-08-29 | GSE60900 | GEO
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:In this study, we tested if miRNAs are altered in amygdala and ventral striatum as a consequence of prenatal ethanol exposure and/or social enrichment. miRNA samples from 72 male and female adolescent rats were analyzed by RNA-Seq analysis and Affymetrix miRNA arrays. Several miRNAs showed significant changes due to prenatal ethanol exposure or social enrichment in one or both brain regions. Some of the miRNA changes caused by ethanol were reversed by social enrichment. The top predicted gene targets of these miRNAs were mapped and subjected to pathway enrichment analysis. We also directly examined the evidence for modulation of target mRNAs in whole transcriptome microarray data from the same rats. Among the pathways most strongly affected were p53, CREB, Glutamate and GABA signaling. Together, our data suggest a number of novel epigenetic mechanisms for social enrichment to reverse the effects of ethanol exposure. A total of 48 samples were analyzed by small RNA-Sequencing using RNA purified from 2 brain regions (amygdala and ventral striatum) of postnatal day 42 Long Evans rats. 3 replicate sequencing runs were performed for each gender within 4 different treatment groups (prenatal ethanol or prenatal saline exposed; postnatal socially-enriched or non-enriched environment)
2014-08-29 | E-GEOD-60900 | biostudies-arrayexpress
Project description:In this study, we tested if miRNAs are altered in amygdala and ventral striatum as a consequence of prenatal ethanol exposure and/or social enrichment. miRNA samples from 72 male and female adolescent rats were analyzed by RNA-Seq analysis and Affymetrix miRNA arrays. Several miRNAs showed significant changes due to prenatal ethanol exposure or social enrichment in one or both brain regions. Some of the miRNA changes caused by ethanol were reversed by social enrichment. The top predicted gene targets of these miRNAs were mapped and subjected to pathway enrichment analysis. We also directly examined the evidence for modulation of target mRNAs in whole transcriptome microarray data from the same rats. Among the pathways most strongly affected were p53, CREB, Glutamate and GABA signaling. Together, our data suggest a number of novel epigenetic mechanisms for social enrichment to reverse the effects of ethanol exposure. A total of 48 Rat ST Gene 1.0 GeneChips and 48 miRNA 2.0 GeneChips were run on RNA purified from 2 brain regions (amygdala and ventral striatum) of postnatal day 42 Long Evans rats. 3 replicate arrays were run for each gender within 4 different treatment groups (prenatal ethanol or prenatal saline exposed; postnatal socially-enriched or non-enriched environment)
2014-08-28 | E-GEOD-60819 | biostudies-arrayexpress