ArticleAlcoholism, clinical and experimental research2019
Resistance of Postnatal Hippocampal Neurogenesis to Alcohol Toxicity in a Third Trimester-Equivalent Mouse Model of Gestational Alcohol Exposure.
Article in Alcoholism, clinical and experimental research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Fluoxetine for Prenatal Alcohol-Exposed Mice: Addressing Impaired Enrichment-Mediated Neurogenesis.bioRxiv : the preprint server for biology · 2026Article
- Adult Hippocampal Neurogenesis as a Therapeutic Target in Fetal Alcohol Spectrum Disorder.Advances in experimental medicine and biology · 2025Review
- Persistent myelin abnormalities in a third trimester-equivalent mouse model of fetal alcohol spectrum disorder.Alcoholism, clinical and experimental research · 2022Article
- Functional and Structural Correlates of Impaired Enrichment-Mediated Adult Hippocampal Neurogenesis in a Mouse Model of Prenatal Alcohol Exposure.Brain plasticity (Amsterdam, Netherlands) · 2020Article
- Early Ethanol Exposure Inhibits the Differentiation of Hippocampal Dentate Gyrus Granule Cells in a Mouse Model of Fetal Alcohol Spectrum Disorders.Alcoholism, clinical and experimental research · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe adult hippocampal dentate is comprised of both developmentally generated dentate granule cells (dDGCs) and adult-generated dentate granule cells (aDGCs), which play distinct roles in hippocampal information processing and network function. EtOH exposure throughout gestation in mouse impairs the neurogenic response to enriched environment (EE) in adulthood, although the basal rate of adult neurogenesis under standard housing (SH) is unaffected. Here, we tested whether the production and/or survival of either dDGCs or aDGCs are selectively impaired following exposure of mice to EtOH vapors during early postnatal development (human third trimester-equivalent), and whether this exposure paradigm leads to impairment of EE-mediated dentate neurogenesis in adulthood.
methodsAll experiments were performed using NestinCreER
resultsEarly postnatal EtOH exposure had no statistically significant effect on the production or survival of tdTom
conclusionsBoth early postnatal dentate neurogenesis and adult dentate neurogenesis, as well as the adult neurogenic response to EE, are surprisingly resistant to early postnatal EtOH vapor exposure in mice.
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Registered trials
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