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Objective Oligodendrocyte precursor cells (OPC) are particularly susceptible to perinatal hypoxia-ischemia resulting in decreased myelination and infant cerebral palsy.The precise mechanism remains unclear.Physiological recordings from these cells have revealed that they possess unique potassium channel properties, which are distinct from the traditional class of glial cell and neuron.This study is to explore whether rectified potassium channel of OPC is involved in hypoxia ischemic brain damage.Methods Whole cell voltage dependent ion channels were recorded by patch clamp technology in acute brain slices of postnatal 7 days rats after hypoxia-ischemia 2 hrs.Every recorded cell, which was injected intracellular Lucifer yellow, was identified with the marker NG2 by fluorescent immunohistochemistry.Results (1) Sodium to potassium conductance ratio was decreased, owing to the increase of inward sodium current amplitude.(2) Outward rectified potassium channel exhibited rectify fall off.(3) There was no significant difference in variable rectified potassium channel and inward rectified potassium channel.(4) Tail current and activation voltage were all raised, which reduced activation and inactivation of potassium channel.Conclusion Outward rectified potassium channel and tail current of potassium channel play more important role in OPC susceptible to hypoxia ischemia.