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- W77239075 abstract "Prenatal alcohol exposure is associated with long-lasting changes in brain structure as well as neurobehavioral dysfunction in humans. The molecular mechanisms underlying these outcomes remain poorly understood. This study used a mouse model of moderate prenatal ethanol exposure, based on voluntary maternal consumption of 10% ethanol from fertilization to mid-gestation, to gain a better understanding of the consequences of moderate ethanol exposure during early pregnancy at both the phenotypic and molecular levels. Hypoactivity was observed in adult mice exposed to ethanol in utero. Males also displayed a disproportionate reduction in hippocampal volume. Gene expression analyses in the adult hippocampus revealed sex- and age-specific up-regulation of solute carrier family 17, member 6 (Slc17a6), which encodes the vesicular glutamate transporter 2 (VGLUT2) protein and is involved in glutamate neurotransmission, following prenatal ethanol exposure. This transcriptional up-regulation correlated with decreased DNA methylation and an enrichment of an active chromatin mark, H3 lysine 4 trimethylation, at the Slc17a6 promoter. In contrast to Slc17a6 transcript levels, VGLUT2 protein levels were significantly decreased in adult ethanol-exposed hippocampi, suggesting post-transcriptional regulation at this locus. Transcriptional profiling of the hippocampus identified a number of ethanol-sensitive microRNAs, and mmu-miR-467b-5p was shown to directly interact with Slc17a6 in an in vitro reporter assay, supporting the idea that it contributed to the reduction of hippocampal VGLUT2. Three other microRNAs, mmu-miR-135a, mmu-miR-135b and mmu-miR-487b were also validated as ethanol-sensitive in the adult male hippocampus, but their target genes remain unknown. These findings demonstrate that moderate prenatal ethanol exposure during early pregnancy can result in long-term phenotypic and molecular changes in adult offspring. They also raise the possibility that some phenotypes observed in fetal alcohol spectrum disorders may be due to altered epigenetic and/or microRNA-based control of glutamate neurotransmission in the hippocampus. Finally, the observation of a correlation between microRNA expression in the hippocampus and serum raises the possibility that ethanol-sensitive circulating microRNAs could be used in the future as biomarkers of gestational ethanol exposure." @default.
- W77239075 created "2016-06-24" @default.
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- W77239075 date "2014-11-06" @default.
- W77239075 modified "2023-09-24" @default.
- W77239075 title "Brain structure and function in a mouse model of moderate prenatal ethanol exposure" @default.
- W77239075 doi "https://doi.org/10.14264/uql.2014.297" @default.
- W77239075 hasPublicationYear "2014" @default.
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