In addition, immunocytochemical and electrophysiological studies have demonstrated that hypoxic preconditioning promotes neural progenitor differentiation and enhances cell survival. Preconditioning is a phenomenon that promotes neuroprotective endogenous mechanisms that prevent future injury by adapting the tissues to low doses of noxious insults. Although not fully elucidated, it is believed that activation of the cell genome and protein synthesis is the general mechanism for inducing brain tolerance by hypoxic preconditioning. Molecules proposed to trigger and sustain the survival, differentiation and plasticity pathways include neuromodulatory peptides; growth factors; as well as the oxygen-sensitive transcription factors HIF-1a and HIF-2a. Understanding how the neonatal brain reacts to injury and which endogenous strategies allow repair and survival is of utmost importance in devising effective therapeutic strategies. Here, we examine whether different hypoxic treatments affect cerebellar development, mainly by studying the expression of NeuroD1 and GAD67 as glutamatergic and GABAergic markers of granule and Purkinje cells, respectively. Birth asphyxia or intrapartum-related neonatal death is globally the 5th most common cause of death among children under 5 years. Survival may result in transient or permanent impairment of cerebellar functions, including motor control and cognitive and affective processes. As there is at present an imperative need for devising Furosemide preventive or palliative therapies for this condition, knowledge of the molecular mechanisms involved is of the utmost importance. Here, we describe a series of disturbances occurring in the cerebellum between the first and second postnatal weeks, during one of the most important periods for the establishment of the fine�Ctuning of performance that include the formation of correct synaptic contacts. During the early postnatal Dyphylline period, the major source of input onto Purkinje cell somata switches from the glutamatergic climbing fibers to the GABAergic basket cell fibers.From P9 to P15 there is a steep decrease in the CF-spine synapses in coincidence with the developmental elimination of perisomatic CF synapses, favouring a monopolized dendritic innervation by a single winner CF.