Developmental white matter injury (DWMI) caused by hypoxia-ischemia (H-I) is associated with permanent neurodevelopmental disabilities such as motor and cognitive deficits in preterm infants. Although selective vulnerability of oligodendrocyte progenitor cells (OPCs) was reported in DWMI, the pathological relevance to functional deficits is not clarified yet. We previously reported that impaired motor function especially in the hindlimb and weak immuno-reactivity to myelin basic protein in the cortex of hindlimb area were shown in the DWMI model rat that was made by H-I (right common carotid artery occlusion followed 6% hypoxia for 1 hour) at P3. To confirm whether corticospinal neurons in the cortex of hindlimb area are intact in the DWMI model, the early marker stainings for neuronal cell death (Fluoro-Jade B staining: FJ-B and Argyophil III staining: A-III) were carried out after H-I. Although FJ-B positive cells were detected in the deep cortex layer (IV-V) in ipsilateral motor-sensory area at 24h after H-I, A-III positive cells were not shown at 6h and 3d later. Additionally, active-capase3 and NeuN double-positive neurons were not detected in the cortex until 48h, indicating that no obvious cell death of neurons occur after H-I. Next, to determine whether indirect damage in the coticospinal neurons is induced after H-I, a retrograde tracer (Fluoro-Gold: FG) was injected into the spinal cord at C3-4 level at P20 and detected 6 days later. FG positive cells in the layer V cortex showed a tendency of the reduction in motor area (77.5 ±3.34 % of contralateral side, p=0.09). Data suggest that distinct cell death in the corticospinal neurons were not induced by H-I directly, but a minor damage of the neurons might be indirectly induced relating to impaired motor function and myelin disturbance in DWMI model rat.