A study has been made of the transplacental passage of thyroxine (T₄) in rats when the hormone is present in physiological concentrations, and of the activity of the foetal thyroid gland in the perinatal period. Several aspects of foetal thyroid function were assessed in intact and thyroid-ectomized (TX) pregnant rats maintained with graded doses of T₄. A daily dose of 2 μg T₄/100 g body weight yielded near normal maternal and foetal serum PBI levels; with a dose of 1 μg the values were slightly low. Both these doses resulted in a decrease in the total and T₄ iodine content of the foetal thyroid; an even greater decrease occurred in rats maintained with 5 μg/100 g body weight/day. The rate of uptake of iodine by the foetal gland was significantly depressed by the 2 but not the 1 μg dose. Serum PBI levels in the foetus were related directly to the dose of T₄ and inversely with the degree of depression of the thyroid gland. Both maternal and foetal serum PBI levels in the unsupplemented TX rats were at least 60 % of normal and there was evidence of increased secretion of T₄ by the foetal thyroid. The data indicate that the placenta is readily permeable to T₄ when the hormone is present in maternal serum in doses that are close to physiological. However it was not possible to estimate the extent of the placental transfer of endogenous hormone. Significant foetal thyroid function was evident near term. It is suggested that both the foetal and maternal thyroids contribute to the maintenance of serum T₄ levels in the foetus.