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Researches have shown that melatonin is neuroprotectant in ischemia/reperfusion- mediated injury. Although melatonin is known as an effective antioxidant, the mechanism of the neuroprotection cannot be explained merely by its antioxidation. Our study was devoted to explore other existing mechanisms by investigating whether melatonin protects ischemia/reperfusion-injured neurons through elevating autophagy, since autophagy has been frequently suggested to play a crucial role in neuron survival. To find it out, an ischemia/reperfusion model in N2a cells was established for examination by MTT, TEM, LCSM and Western Blotting. The results showed that autophagy was significantly enhanced in N2a cells treated with melatonin at reperfusion onset following ischemia and cell viability was remarkably increased, while autophagy blockage by 3-MA led to decreased N2a cell survival. Besides, classic antioxidant Vitamin C was not as strong as melatonin in promoting cell survival. It was also observed that rapamycin, an autophagy activator, greatly activated autophagy but did not promote cell survival as did melatonin. Taken together these data suggest that in addition to antioxidation, autophagy is possibly one of the mechanisms underlying neuroprotection of melatonin.