Objective: Electroacupuncture(EA) has been reported to be effective for treating depression.The purpose of this study was to explore the mechanism of EA’s function on the expression of brain-derived neurotrophic factor(BDNF), which is known to be associated with depressive disorders.Methods: A rat model of depression induced by chronic stress was established by alternating the following methods, water-break(24 h), night light(12 h), swimming(4 ℃, 5 min), shaking(30 min) and bounding(3 h), every day for four weeks.Rats were randomly divided into six groups(n=10 each): normal, normal+hand acupuncture, model, model+acupuncture, model+hand acupuncture, and model+paroxetine.EA was given at acupoints Baihui(GV20), Yintang(GV29) and Neiguan(PC6) for 10 min(2/100 Hz alternating, 0.2 mA) every other day for four weeks.The rats were decapitated and the brain tissues were collected after four weeks of treatment.Westernblot method was used to test BDNF in hippocampus and prefrontal cortex.Results: Compared to the normal group, protein expression of BDNF significantly decreased in the model group(P<0.01) in the hippocampus and prefrontal cortex.In the hippocampus: compared with the model group, the hand acupu ncture group andthe EA group obviously increased(P<0.01), and the paroxitine group increased(P<0.05); In the prefrontal cortex: compared with the model group, the hand acupuncture group, the EA group and the paroxitine group obviously increased(P<0.01).BDNF expression increased in the model+hand acupuncture group and the model+paroxitine group compared with the model group(P<0.01) and in the model+hand acupuncture group compared with the mode+EA group(P<0.01).Conclusion: Solitary combined with chronic stress can significantly reduce the expression of BDNF.Hand acupuncture, EA and paroxetine intervention can improve the expression level of BDNF.Acupuncture treatment has obvious advantages in raising BDNF protein expression level.These indicated that acupuncture can alleviate depression through stimulating the Ras-MAPK-ERK pathway and expanding protein expression of BDNF to protect the neurons.