Role of early migratory neural crest cells in developmental anomalies induced by ethanol.

The purpose of this work was to study the dispersion of early migratory neural crest cell (NCC) of chick embryos treated with ethanol concentration known to induce the Fetal Alcohol Syndrome (FAS). After a direct treatment with ethanol (250 mg/dl), there was a higher number of abnormal embryos than in the control group, showing neural and cardiac anomalies. After NC-1 immunostaining, ethanol-treated embryos showed smaller number of NCC at all neuraxis levels and presumptive NCC were frequently seen flowing towards the lumen of the neural tube. Present data support the view that ethanol impairment of migratory behaviour of NCC may explain certain anomalies of FAS such as those found at the cephalic end of the body, which is known to be largely derived from NCC.