Experimental dysraphism in the rat.

Abstract

An experimental treatment that results in dysraphic lesions in rat embryos was studied to gain insight into the origin of such lesions. Pregnant rats given 100,000 units of vitamin A by gavage tube on gestational Days 8, 9, and 10 produced abnormal litters, and 50% of the embryos had exencephaly and/or spina bifida. Study of these embryonic lesions revealed hyperplesia of neural tube tissue that extended laterally to the edge of an epidermal defect. The epidermal defect consisted of the absence of fetal epidermis over the hyperplastic neural tissue. At no stage in development was embryonic hydrocephalus noted. In fact, the central canals of the embryos with malformations were poorly developed and smaller than those of control embryos. Results with this model indicate that the malformations arise through a process of overgrowth and hyperplasia and not from embryonic hydrocephalus. Continued work with this and other models is required to delineate new mechanisms and to offer alternative postulates for the origin of dysraphic lesions.