More recently, magnetic resonance imaging studies have provided a complete overview of the effects of severe hypoxia-ischemia in both preterm and term neonates. Deep gray matter injury with peri-Rolandic involvement is more frequently observed in the older age group. Less profound insults Eltrombopag result in intraventricular hemorrhages and periventricular white matter injury in preterm neonates and parasagittal watershed territory infarcts in term neonates. In the postnatal period, severe insults result in diffuse GM injury, with relative sparing of the periRolandic cortex and the structures supplied by the posterior circulation. Profound hypoxia-ischemia in older children and adults BV6 affects the GM deep nuclei, cerebral cortices, hippocampi and cerebellum. Thus, many critical neuronal populations at different maturation stages are at great risk during ischemic insults, for example projection neurons in the deep nuclei of the brainstem. Peng et al. pointed out that following focal cerebral hypoxic-ischemic injury, neuronal apoptosis accompanying necrosis occurs in the cerebellum, an area outside the vascular supply of the relevant ipsilateral hemisphere. Later on it was found that hypoxia-ischemia at P2, the rat equivalent of human prematurity, cause damage to a subset of Purkinje cells, a significant decrease in the number of interneurons and in the thickness of molecular and granular layers. The neurons of the anterior cerebellum, which are less mature than the ones located in the posterior cerebellum, showed higher vulnerability. Therefore, in order to increase our understanding of the sequelae of asphyxia in the human perinatal period when the cerebellum is still developing, it is important to characterize in detail the effects in animal models. The cerebellum is derived from the neuroepithelium that surrounds the lateral recess of the IVth ventricle in the pons and the medulla, and its formation spans embryonic and postnatal development. Despite its morphological and functional complexity, the on-going developmental processes that take place in the rat postnatal period make cerebellum an attractive and accessible model for perinatal hypoxia-ischemia.