Background Oligodendrocyte progenitor cells (OPCs) are susceptible to perinatal hypoxia ischemia brain damage (HIBD), resulting in infant cerebral palsy due to the effects on myelination.The origin of OPC vulnerability in HIBD remains controversial.Methods In this study, we defined the HIBD punctate lesions by MRI diffuse excessive high signal intensity in postnatal 7 day rats.The coronal and sagittal T2-weighted MRI demonstrated an approximate area of cerebral pathological malformation in HIBD.The electrophysiological functional properties of OPCs were recorded by patch clamp recording in acute cerebral cortex slices.Recorded cells in the slices were intracellularly injected with Lucifer yellow and immunohistochemically labeled with NG2 antibodyto identify local OPCs.