Maternal exposure to methylmercury causes an impairment in ependymal cilia motility in the third ventricle and dilation of lateral ventricles in mice offspring.

Abstract

Although maternal MeHg-exposure causes hydrocephalus in the offspring of mice, its pathogenesis has not been fully explained. In the present study, we examined the issue of how maternal MeHg-exposure in mice affects ependymal ciliary movement in the offspring and whether the lateral ventricles in offspring show dilation. Pregnant mice were given drinking water containing 0, 10, or 20 mg/L MeHg, or a single dose of 2 mg/kg MeHg. Brain slices were prepared from the offspring and the ependymal ciliary movement of ependymal cells in the third ventricle were observed by a high-speed digital camera. The dilation of the lateral ventricles in the offspring was assessed by histological examination. The administration of MeHg in the drinking water of pregnant mice at levels of 10 mg/L and 20 mg/L MeHg from GD10 to birth caused a significant decrease of ciliary beating frequency (CBF) in ependymal cells of the third ventricle in the weaned offspring. The ependymal ciliary movement of the weaned offspring was particularly sensitive in the case of the administration of MeHg at GD10. Moreover, there was a significant dilation of cross-sectional areas of lateral ventricles in weaned offspring from the pregnant mice that had been administered MeHg. The CBF and the cross-sectional areas of the lateral ventricles improved with time. These results suggest that the impairment of ependymal ciliary movement by maternal MeHg-exposure contributes to the development of hydrocephalus in the offspring.