Intracerebral hemorrhage (ICH) can cause direct brain injury at the insult site and indirect damage in remote brain areas. Although a protective effect of melatonin (ML) has been reported in ICH, its detailed mechanisms and effects on remote brain injury remain unclear. To clarify the mechanism of indirect neuroprotection after ICH, we first investigated whether ML improved motor function after ICH and then examined the underlying mechanisms. We made the internal capsule hemorrhage model rat by collagenase injection (15 U/ml, 1.4 µl) near the internal capsule and oral intake of ML (15 mg/kg) was given for a successive 7 days. ML oral administration for 7 days after ICH (D7) resulted in significant recovery of motor function. Injection of a retrograde tracer, Fluoro-Gold (FG), to the corticospinal tract at C3-4 revealed that FG-positive cells in the cortex at 1.7 mm anterior to the bragma (forelimb area) was increased in ML-treated group. To reveal electrophysiological evidence for better function by ML. measurements of motor map in ipsilateral motor cortex were done by intracortical microstimulation (ICMS), in which bipolar pulses (0.2 ms, 0-200 µA, 333 Hz) were given in layer V sensorimotor cortex to evoke twitches in contralateral lower leg joints. Threshold to evoke the muscle twitches was increased after ICH. ICMS revealed that ML treatment results in lower threshold for evoking forelimb movement than control. Data suggested that oral ML administration to ICH model rats reduces the damage of peri-hematoma area including corticospinal pathway by scavenging radicals, resulting in better functional recovery that is confirmed by ICMS.