The clinical continuum of fetal alcohol spectrum disorder (FASD) ranges from craniofacial dysmorphology and mental retardation to the much more common spectrum of developmental learning and behavior disorders.
This study illustrates that neuroanatomical sequelae of fetal ethanol exposure are dose-responsive and suggests that there may be a threshold for this effect.Įxposure to ethanol in utero is recognized as a leading cause of preventable developmental disorder. Both correlations were consistent with linear dose-response models. There were also significant correlations between DCX population in the dentate gyrus and daily dose ( r 2 = 0.560). We report here significant neuronal deficits in the hippocampus with a significant negative correlation between daily dose and neuronal population in CA1 ( r 2 = 0.486), CA2 ( r 2 = 0.492), and CA3 ( r 2 = 0.469). Design-based stereology was performed on cresyl violet-stained and doublecortin (DCX)-immunostained sections of the hippocampus. In the present study, we examined these same parameters in 12 FAE offspring with a similar average but a larger range of ethanol exposures (1.01–2.98 g/Kg/day total ethanol exposure 24–158 g/Kg). Fetal alcohol-exposed (FAE) offspring also showed significantly lower volumes for these structures at 2 years of age. We previously reported that 2-year-old offspring of vervet monkey ( Chlorocebus sabeus) dams drinking, on average, 2.3 ± 0.49 g ethanol per Kg maternal body weight 4 days per week during the last third of pregnancy had significantly lower numbers of CA1 (−51.6%), CA2 (−51.2%) and CA3 (−42.8%) hippocampal neurons, as compared to age-matched sucrose controls.
Fetal alcohol spectrum disorder (FASD) is a chronic debilitating condition resulting in behavioral and intellectual impairments and is considered the most prevalent form of preventable mental retardation in the industrialized world.
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