International Journal of Developmental Neuroscience · 1992 · 127 citations · 20 references
Life SciencesDevelopmental BiologyNeuroscienceDevelopmental NeuroscienceEmbryogenesisEmbryologyDevelopmental NeurotoxicologyNeural DevelopmentNeurodevelopmental ToxicityNeurogenesisNeuronal Cell DeathNeurotoxic MechanismsAcute Ethanol IntoxicationAlcohol-related Developmental ToxicityAlcohol-related Neurodevelopmental DamageNeural Tube EmbryologyNeural Tube FormationNeural Tube MorphogenesisOtic Placode DevelopmentTeratogenic Effects Of Alcohol
Vital staining and routine histological analyses of mouse embryos 12 h after acute maternal ethanol administration (2.9 g/kg) illustrated that selected neuronal cell populations are killed. At the time of treatment, embryos had 5-15 somite pairs, corresponding to the developmental stages occurring in humans during the fourth week of post-fertilization; i.e. when neural folds are present and neural tube fusion begins. Affected cell populations in embryos having 6-26 somite pairs (up to the stage of anterior neuropore closure) were in discrete locations in the alar and basal plates of the rhombencephalon, in the otic placode/vesicle, and in the regions of the epibranchial placodes, olfactory placodes and trigeminal ganglion. The potential basis for the vulnerability of these cell populations to ethanol-induced cell death is discussed. Our understanding of the scope of ethanol-induced CNS damage is dependent upon further defining ethanol-sensitive cell populations at all stages of CNS development.
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RECOGNITION OF THE FETAL ALCOHOL SYNDROME IN EARLY INFANCY
KennethL. Jones, DavidW. Smith · The Lancet · 1973 · 2.8K citations
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