Structure and histogenesis of the principal sensory nucleus of the trigeminal nerve: effects of prenatal exposure to ethanol.

Clinical and experimental evidence shows that prenatal exposure to ethanol causes craniofacial malformations, microcephaly, and abnormal development of the central nervous system. This study describes the effects of ethanol on the development of the principal sensory nucleus of the trigeminal nerve (PSN). The offspring of two groups of rats were examined. Pregnant females in one group were fed a liquid diet containing 6.7% (v/v) ethanol (Et) and rats in the other group were fed an isocaloric liquid control diet (Ct). Each pregnant rat was administered [3H]thymidine on one day during the period from gestational day (G) 10 to G22. After pups grew to 30 days of age, they were killed and their brains were processed by an autoradiographic procedure. Qualitatively, the PSN of Ct- and Et-treated rats appeared similar; they were composed chiefly of small neurons and a few scattered large neurons. On the other hand, quantitative analyses revealed significant differences between both groups. Although the volume of the PSN of Et-treated rats was not significantly different (-3.2%) than that for Ct-treated rats, the PSN of Et-treated rats had significantly (P less than 0.01) fewer (30.0%) neurons than did the PSN of Ct-treated rats. The number of the small neurons, but not of the large neurons, was affected most by the ethanol exposure. Prenatal exposure to ethanol also altered the generation of PSN neurons. Most neurons in the PSN of Ct-treated rats were born between G12 and G15, the small neurons being generated before the large neurons. In Et-treated rats, too, small neurons were born before the large neurons; however, the time frame of neuronogenesis was delayed as it occurred between G13 and G16. Thus, prenatal exposure to ethanol produces profound developmental abnormalities that lead to permanent alterations in the structure of the mature central nervous system.