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Updated: Sep 23, 2025
Construction of Vapor Chambers Used to Expose Mice to Alcohol During the Equivalent of all Three Trimesters of Human Development
Published on: July 13, 2014
Oligodendrocyte lineage is severely affected in human alcohol-exposed foetuses
Florent Marguet1, Mélanie Brosolo2, Gaëlle Friocourt3
1Department of Pathology, Normandy Centre for Genomic and Personalized Medicine, Laboratoire d'Anatomie Pathologique, Pavillon Jacques Delarue, CHU, Normandie Univ, UNIROUEN, INSERM U1245 and Rouen University Hospital, 1 Rue de Germont, 76031, Rouen Cedex, France. florent.marguet@hotmail.fr.
Insights
Prenatal alcohol exposure significantly impacts brain development, increasing oligodendrocyte precursor cells and decreasing mature cells. This suggests a major impairment in oligodendrocyte lineage during fetal development.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- Prenatal alcohol exposure is a leading cause of neurodevelopmental disabilities.
- Human studies link alcohol to white matter anomalies, but primarily postnatally, with limited prenatal oligodendrocyte lineage data.
- Rodent studies indicate alcohol impairs oligodendrocyte differentiation, highlighting a need for human fetal data.
Purpose of the Study:
- To investigate the antenatal effects of prenatal alcohol exposure on oligodendrocyte precursor cells (PDGFR-α+) and immature/mature oligodendrocytes (Olig2+) in the human fetal brain.
- To compare these cell populations in alcohol-exposed fetuses with age-matched controls between 15 and 37 weeks gestation.
Main Methods:
- Immunohistochemistry was used to analyze PDGFR-α and Olig2 expression in the ganglionic eminences and frontal cortex of 14 human fetuses.
- Brains were obtained from fetal autopsies following medical termination of pregnancy or early demise.
Main Results:
- PDGFR-α expression was significantly increased in the ganglionic eminences and cortex of alcohol-exposed fetuses (except at the earliest stage).
- No substantial increase in Olig2-positive cells was observed in the ganglionic eminences by late gestation in exposed fetuses.
- Olig2-positive cell density was consistently lower in the frontal cortex of alcohol-exposed fetuses compared to controls.
Conclusions:
- Prenatal alcohol exposure causes significant oligodendrocyte lineage impairment during critical fetal brain development stages.
- Findings suggest defective or delayed generation and maturation of oligodendrocyte precursors and cells in exposed human fetuses.
- These antenatal alterations provide evidence for the mechanisms underlying alcohol-related neurodevelopmental disabilities.
Abstract:
Prenatal alcohol exposure is a major cause of neurobehavioral disabilities. MRI studies in humans have shown that alcohol is associated with white matter microstructural anomalies but these studies focused on myelin abnormalities only after birth. Only one of these studies evaluated oligodendrocyte lineage, but only for a short period during human foetal life. As data are lacking in humans and alcohol is known to impair oligodendrocyte differentiation in rodents, the present study aimed to compare by immunohistochemistry the oligodendrocyte precursor cells expressing PDGFR-α and immature premyelinating/mature oligodendrocytes expressing Olig2 in the ganglionic eminences and the frontal cortex of 14 human foetuses exposed to alcohol from 15 to 37 weeks' gestation with age-matched controls. The human brains used in this study were obtained at the time of foetal autopsies for medical termination of pregnancy, in utero or post-natal early death. Before birth, PDGFR-α expression was strongly increased in the ganglionic eminences and the cortex of all foetuses exposed to alcohol except at the earliest stage. No massive generation of Olig2 immunoreactive cells was identified in the ganglionic eminences until the end of pregnancy and the density of Olig2-positive cells within the cortex was consistently lower in foetuses exposed to alcohol than in controls. These antenatal data from humans provides further evidence of major oligodendrocyte lineage impairment at specific and key stages of brain development upon prenatal alcohol exposure including defective or delayed generation and maturation of oligodendrocyte precursors.
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