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Fetal Alcohol SyndromeEye Malformations in a Mouse Model
Cynthia S. Cook, DVM, MS;
Andrea Z. Nowotny, MD;
Kathleen K. Sulik, PhD
Arch Ophthalmol. 1987;105(11):1576-1581.
Abstract
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Acute maternal ethanol administration on gestational day 7 (gastrulation stage) in C57BI/6J mice results in a spectrum of ocular malformations. A deficiency in the anterior neural plate observable within 24 hours of exposure results in corresponding defects in the optic sulcus and subsequent optic vesicle. Deficiency in the size of the lens vesicle induced by a small optic vesicle is demonstrable as microphakia in older embryos. Delayed detachment of the lens vesicle from the surface ectoderm manifests in the live offspring as progressive corneal opacification and vascularization related to defects in corneal endothelium and Descemet's membrane. Anterior segment dysgenesis results in persistent iridocorneal adhesions, dyscoria, and abnormal formation of the anterior chamber. In contrast, ethanol exposure on day 8 of gestation did not result in eye malformations. Thus, it appears that many of the ocular abnormalities associated with fetal alcohol syndrome may result from an acute insult to the optic primordia during a very specific period that corresponds to the third week after fertilization in the human.
Author Affiliations
From the Departments of Anatomy (Drs Cook, Nowotny, and Sulik) and Ophthalmology (Dr Sulik), School of Medicine, University of North Carolina, Chapel Hill.
Footnotes
Accepted for publication July 17, 1987.
Reprint requests to Department of Anatomy, Swing Building, School of Medicine, University of North Carolina, Chapel Hill, NC 27514 (Dr Cook).
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