Abstract
Optic nerve hypoplasia is an important malformation of the fetal alcohol syndrome whose teratogenic mechanisms are unknown. In our experimental model we have quantified the concentration of ethanol and acetaldehyde in the retina and vitreous humor of the developing chick. The effect of ethanol alone during retinal development was analyzed by conventional histological techniques and by immunostaining. A single injection of ethanol in the vitelline sac at the beginning of retinal cell differentiation retarded synaptogenesis in the inner plexiform layer and produced abundant ganglion cell death and a sharp diminution of myelinic axons. Our observations could help to explain certain alterations described in children exposed to ethanol during the development of their nervous system.
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