ArticleGene expression2008
Ethanol exposure during neurogenesis induces persistent effects on neural maturation: evidence from an ex vivo model of fetal cerebral cortical neuroepithelial progenitor maturation.
Article in Gene expression, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 82 citations in OpenAlex.
- Reduced fetal cerebral blood flow predicts perinatal mortality in a mouse model of prenatal alcohol and cannabinoid exposure.BMC pregnancy and childbirth · 2024Article
- Sex differences in the transcriptome of extracellular vesicles secreted by fetal neural stem cells and effects of chronic alcohol exposure.Biology of sex differences · 2023Article
- Alcohol & cannabinoid co-use: Implications for impaired fetal brain development following gestational exposure.Experimental neurology · 2023Review
- Ethanol-induced cerebellar transcriptomic changes in a postnatal model of fetal alcohol spectrum disorders: Focus on disease onset.Frontiers in neuroscience · 2023Article
- Article
- Prenatal alcohol exposure contributes to negative pregnancy outcomes by altering fetal vascular dynamics and the placental transcriptome.Alcoholism, clinical and experimental research · 2022Article
- Gag-like proteins: Novel mediators of prenatal alcohol exposure in neural development.Alcoholism, clinical and experimental research · 2022Article
- Cell type-specific changes in Wnt signaling and neuronal differentiation in the developing mouse cortex after prenatal alcohol exposure during neurogenesis.Frontiers in cell and developmental biology · 2022Article
- Divergent and overlapping hippocampal and cerebellar transcriptome responses following developmental ethanol exposure during the secondary neurogenic period.Alcoholism, clinical and experimental research · 2021Article
- Cell-type and fetal-sex-specific targets of prenatal alcohol exposure in developing mouse cerebral cortex.iScience · 2021Article
- Dose-response analysis of microvasculature changes in the murine fetal brain and the maternal extremities due to prenatal ethanol exposure.Journal of biomedical optics · 2020Article
- Article
- CCL2/CCR2 system in neuroepithelial radial glia progenitor cells: involvement in stimulatory, sexually dimorphic effects of maternal ethanol on embryonic development of hypothalamic peptide neurons.Journal of neuroinflammation · 2020Article
- Embryonic Ethanol Exposure Affects the Early Development, Migration, and Location of Hypocretin/Orexin Neurons in Zebrafish.Alcoholism, clinical and experimental research · 2019Article
- Ethanol Exposure Increases miR-140 in Extracellular Vesicles: Implications for Fetal Neural Stem Cell Proliferation and Maturation.Alcoholism, clinical and experimental research · 2019Article
- Subventricular zone neural precursor cell responses after traumatic brain injury and binge alcohol in male rats.Journal of neuroscience research · 2019Article
- Evaluating the effects of maternal alcohol consumption on murine fetal brain vasculature using optical coherence tomography.Journal of biophotonics · 2018Article
- Epigenetic mediators and consequences of excessive alcohol consumption.Alcohol (Fayetteville, N.Y.) · 2017Review
- DNA Methylation program in normal and alcohol-induced thinning cortex.Alcohol (Fayetteville, N.Y.) · 2017Article
- Postnatal choline supplementation selectively attenuates hippocampal microRNA alterations associated with developmental alcohol exposure.Alcohol (Fayetteville, N.Y.) · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Ethanol is a significant neuroteratogen. We previously used fetal cortical-derived neurosphere cultures as an ex vivo model of the second trimester ventricular neuroepithelium, and showed that ethanol directly induced fetal stem and progenitor cell proliferation and maturation without inducing death. However, ethanol is defined as a teratogen because of its capacity to persistently disrupt neural maturation beyond a specific exposure period. We therefore utilized a simplified neuronal maturation paradigm to examine the immediate and persistent changes in neuronal migration following ethanol exposure during the phase of neuroepithelial proliferation. Our data indicate that mRNA transcripts for migration-associated genes RhoA, Paxillin (Pxn), and CDC42 were immediately induced following ethanol exposure, whereas dynein light chain, LC8-type 1 (DYNLL1), and growth-associated protein (Gap)-43 were suppressed. With the exception of Gap43, ethanol did not induce persistent changes in the other mRNAs, suggesting that ethanol had an activational, rather than organizational, impact on migration-associated mRNAs. However, despite this lack of persistent effects on these mRNAs, ethanol exposure during the proliferation period significantly increased subsequent neuronal migration. Moreover, differentiating neurons, pretreated with ethanol during the proliferation phase, exhibited reduced neurite branching and an increased length of primary neurites, indicating a persistent destabilization of neuronal maturation. Collectively, our data indicate that ethanol-exposed proliferating neuroepithelial precursors exhibit subsequent differentiation-associated increases in migratory behavior, independent of mRNA transcript levels. These data help explain the increased incidence of cerebral cortical neuronal heterotopias associated with the fetal alcohol syndrome.
Indexed as
Identifiers
18590052PMC2925251W28589715What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.