Somite necrosis and developmental malformations induced by vitamin A in the golden hamster

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Abstract
A simple method for the induction of developmental malformation in the golden hamster is presented. The teratogenic agent used consists of a single dose of vitamin A. Correlations between the day of gestation at which the vitamin A is administered and the type and percentage of malformations induced are reported. Young embryos obtained from treated mothers on the 8th day of gestation show somite necrosis within 12 hr. of the administration of vitamin A, reaching its maximum at 24 hr. The somite necrosis is considered to be a basic alteration resulting in an abnormal axial mesoderm which then fails to fulfil its function of lodging and protecting the neural tube. The unprotected and exposed neural tissue secondarily degenerates. Somite necrosis is considered to be the primary defect induced by vitamin A causing developmental malformations such as cranioschisis and sacral rachischisis. When somite necrosis occurs before neural tube closure extensive degeneration of the neural tube follows (e.g. cranioschisis). Somite necrosis occurring after closure of neural tube results in only minimal change in the neural tube (e.g. occult sacral rachischisis). Notochordal alterations (hypertrophy and necrosis) are also found in the young hamster embryo after administration of vitamin A to their mother on the 8th day of gestation.