Neonatal hypothyroidism in rats resulted in a decrease in the rate of cerebellar cell division and a delay in the time when cell division ceased. Thus, by 35 days total cell number, as measured by DNA content, was normal. The prolongation of cell division was reflected by an elevation of DNA polymerase activity that persisted beyond the time enzyme activity dropped to adult levels in either normal animals or animals equally retarded in their growth by malnutrition. This increase in polymerase activity was associated with a sevenfold increase in tritiated thymidine incorporation into DNA at 21 days of age. These findings support the view that the effects of hypothyroidism on the timing of cell proliferation in the cerebellum are not mediated solely by the well-known decrease in food intake that occurs in hypothyroidism and that might be expected to result in some degree of malnutrition.