Several classes of finely interconnected neurons located in the cortex and deep nuclei contribute to cerebellar complexity. The glutamatergic Go6976 granule cells and the GABAergic Purkinje cells represent the two main cell types analyzed in this study. The granule cells are Amifostine important cerebellar interneurons that originate in the cortical external germinative layer, which derives from a neurogenic zone called the rhombic lip. In the rat EGL, granule cell neurogenesis extends from P4 to P19 with a maximum between P8 and P15. Thus proliferation, radial migration into the cerebellar cortex along the processes of the Bergmann glia cells, differentiation, and settling mechanisms that give rise to the granule cells all take place during the period of the model of brain injury and/or hypoxic preconditioning described here. The time course of human cerebellar granule cell origin is less well defined, starting in the fetal period and ending in a variable range from the 7th postnatal month to the end of the 2nd year. The Purkinje cells, the cerebellar output neurons with axons that project out of the cortex mainly towards the deep cerebellar nuclei, originate from a germinal niche in the roof of the IVth ventricle much earlier than the granule cells, with a neurogenic peak at E15 in rat and around the 6th week after fertilization in human. Despite the neurogenic gap between granule and Purkinje cell populations, it has been shown that the terminal differentiation of rat Purkinje cells during the 2nd and 3rd weeks after birth is highly dependent on interactions with the Bergmann glia and cerebellar interneurons, including the granule cells and their parallel fibers. This late stage in Purkinje cell differentiation involves specific features of dendritic arborization and orientation, amongst others. Two molecular markers have been chosen in this study to evaluate the effects of global and/or ischemic hypoxia on the developing cerebellum, a transcriptional factor known as NeuroD1/BETA2 and the GABAergic enzyme GAD67. The pro-neuronal role of NeuroD1 was first reported in Xenopus after ectopic expression that leads to neuron formation from the ectoderm.