Treatment with Iodine in Pregnant Rats with Marginal Iodine Deficiency Improves Cell Migration in the Developing Brain of the Progeny

Marginal iodine deficiency is a common health problem in pregnant women. Epidemiological and animal studies had shown that marginally maternal iodine deficiency could cause the mild changes of maternal thyroid function, eventually lead to a negative effect on neurodevelopment. But the underlying mechanisms responsible for the neurological impairment remain unclear. The aim of this study is to explore whether marginally maternal iodine deficiency could produce subtle changes in cell migration and cognitive function of offspring, and the optimal time of giving intervention to minimize the adverse effects. In the present study, we established a marginal iodine deficiency model, and iodine supplement was performed on pre-pregnancy (PP), G13 (gestation day 13), and postnatal day 0 (P0). Our data showed that there were changes in the cytoarchitecture and the percentage of bromodeoxyuridine (BrdU)-labeled cells in the cerebral cortex in marginal iodine deficiency rats. The Reelin expression was significantly lower, but Tenascin-C was higher in the cerebral cortex of marginal iodine deficiency group on P7 than the normal group, respectively. When iodine supplement, especially before G13 could reverse the abnormal expression of the two proteins involved in cell migration, which was consistent with the results of Morris Water Maze test. The three intervention groups had shorter escape latencies than the marginal iodine deficiency rats. The earlier that iodine is supplied, the better behavior performance would reach. Our findings suggested that iodine supplement in early stage of pregnancy could improve the cell migration of cerebral cortex and neurodevelopment of offspring.