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Abstract

The principal features of fetal alcohol syndrome (FAS) include microcephaly, reduced body size, and characteristic facial malformation, most of which are associated with hypoplasticity of structures around the mouth. A recent study using pregnant mice suggested that the malformations in FAS are caused by the effects of ethanol on early embryos during gastrulation and neurulation. Exposure of Xenopus laevis early embryos to 1–2% ethanol until they developed to the late neurula stage produced craniofacial malformations in tadpoles which have many similarities with the described features of FAS. They include reduced length of brain, reduced body size, and hypoplasticity of the anterior end of the body around the mouth. Size reduction from the control group was about 20% in the mouth region, and 10% in other head regions. Ethanol inhibited migration of mesodermal cells toward the animal pole during gastrulation, thus inducing a smaller neural plate with reduced anterior—posterior length. These very early effects of ethanol in development seem to produce various craniofacial malformations in tadpoles, and possibly also in human infants with FAS. In contrast to mammalian embryos, one can conveniently study in detail the effects of ethanol on morphogenetic movements in various in vitro experiments by using a large number of amphibian embryos. Thus, amphibian embryos represent a valuable animal model for the study of mechanisms of the teratogenic effects of ethanol.