Thyroid hormone plays a critical role in development of central nervous system, such as neurogenesis, synaptogenesis and myelination. However, little is known about the role of the thyroid hormone during the perinatal period in the development of the mammalian circadian clock located in the hypothalamic suprachiasmatic nucleus (SCN). In this study, we examined the effects of the pharmacological insufficiency of thyroid hormone in the perinatal period on the wheel-running circadian rhythm in the adulthood as well as the gene expression in the neonatal SCN of mice. The pregnant mice were given antithyroid agents from ED17 to 14th day after the delivery and their offspring was normally grown and treated as congenic hypothyroid (CH) mice. CH mice at 8 wk ages showed the shorter period in the circadian behavioral rhythm in the constant darkness compared with control mice. The period of Per2::luciferase reporter rhythm in the explant SCN culture was shorter in CH mice than that from control mice. The mRNA expression of Sox2 gene, which is known to be critical for the normal development of the SCN clock, was upregulated in CH mice. Furthermore, the daily administration of thyroxin all ameliorated the phenotype in CH mice. These results impact the important roles of thyroid hormone in the circadian clock development.