Pregnant rats were administered a teratogenic dose of vitamin A excess on Days 14 and 15 of gestation. Intubation controls received the vehicle alone; nontreated mothers were not disturbed; all groups were fostered to untreated mothers after birth. Treated offspring showed a generalized retardation in growth as evidenced by delayed onset of fur growth, eye‐opening, and reduced body weight. Treated subjects acquired the operant S+, S− discrimination during adulthood significantly slower than the controls because of a failure to inhibit responding in S−. Although their proportion of S+ responding eventually reached the level of the controls, they failed to acquire comparably long S− latencies, even during 40 sessions when S− responding was punished with shock. The treated rats evidently were less able to inhibit responding in the signal which indicated nonreinforcement. Histological examination of the brains revealed that the maternal vitamin A excess produced an overall reduction in offspring brain size with obvious microcephaly occurring in 1 animal.
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Hutchings et al. (1973) studied this question.
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