Chronic hypoxia is a major cause that increases neonatal mortality in the perinatal period. Vascular endothelial growth factor (VEGF) and its receptors induced by hypoxia are increased blood vessel permeability in the developing central nervous system and characterized as a critical factor in angiogenesis and vasculogenesis. This study investigated the development of the rat cerebellum with expression of VEGF and its receptors under chronic hypoxia in compare with normoxia. In addition, this study can contribute to the understanding of the effect development in the postnatal cerebellum. Rat pups were divided into two groups, normoxia and hypoxia group. The cerebellum of 35-day-old rat was removed and prepared for immunofluorescent staining. After staining, the sections were observed under the fluorescent microscope and were taken the picture using the microscopic-digital camera system. Expression of VEGF and Flk-1 restricted only to Purkinje cells, but feline sarcoma virus-like tyrosine kinase-1 (Flt-1) did not express in all of cerebellar layers. Under chronic hypoxia, expression of VEGF and fetal liver kinase-1 (Flk-1) increased in Purkinje cells but no changes in case of Flt-1. These results suggest that the source of VEGF and Flk-1 is Purkinje cells in the cerebellum. And increase of VEGF and Flk-1 expression in the murine cerebellum results from adaptive responses to chronic hypoxia.