In order to reveal mechanisms of brain damages resulted from fluoride toxicity, we treated adult female mice of Swiss Albinos strain by 500 ppm NaF (226 ppm F?) in their drinking water from the 15th day of pregnancy until the day 14 after delivery. All mice were sacrificed on day 14 after parturition. During treatment, levels of thiobarbituric acid reactive substances (TBARS), the marker of lipid peroxidation extend, increased, while the activities of the antioxidant enzymes such as glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT), and the level of glutathione (tGSH) decreased significantly in both cerebellum and cerebrum compared with those of the control group. These results suggested that fluoride enhanced oxidative stress in the brain, thereby disturbing the antioxidant defense of nursing pups. In addition, acetylcholinesterase (AChE) activity in both cerebellum and cerebrum was inhibited after treatment with fluoride. In our previous studies we have found, a decrease in plasma thyroid hormone levels of nursing pups whose mothers were treated by NaF. In cerebellum of mice, migration of neurons from the external granular layer to the internal granular layer occurred postnatally and was dependent upon the presence of thyroid hormone. In hypothyroidism, several neurons failed to complete their migration and died. Key guidance signals to these migrating neurons were provided by laminin, an extracellular matrix protein fixed to the surface of astrocytes. In the present study we examined the expression and distribution of laminin in cerebellum of 14-day-old mice. Immunoreactive laminin was disappeared by postnatal day 14 in cerebellum parenchyma of control pups and was restricted to vasculature despite the continued presence of granular cells in the external granular layer. In contrast, in cerebellum of NaF treated pups, laminin was deposited in organised punctuate clusters in the molecular layer. These data indicated that the disruption of laminin distribution might play a major role in the profound derangement of neuronal migration observed in cerebellum of NaF treated pups.