Objective To observe the effect of vinpocetine on monoamine transmitters in cerebral of poststroke depression (PSD)rats and to investigate the mechanism of pharmacotherapeutics on PSD. Methods Rats were divided randomly into the sham-operated group,the normal saline group,the low dose of vinpocetine group and the high dose of vinpocetine group. Giving the left middle cerebral artery occlusion, the PSD rat model was established by unexpected chronic mild stress. When the PSD rat model was established, vinpocetine group was given vinpocetine(5mg/kg, 10mg/kg) and the normal saline group was given normal saline. Then the ethological score of depression was evaluated on 14 and 28 days. The monoamine transmitter in the frontal cortex and hippocampus and brainstem were detected by the fluorospectrophotometry. Results On the 28th day after the model establishment,compared with the normal saline group, the ethological score of depression level was decreased obviously. Compared with the normal saline group, vinpocetine could improve the ethological score of depression level of the PSD rat model, and these concentrations of 5-hydoxytrypatarmine ( 5-HT), noradrenalin ( NE ) and dopamine ( DA ) in the frontal cortex, hippocampus and brainstem. The level of NE ( ( 192.4 ± 34.8 ) ng/g, ( 206. 0 ± 41.7 ) ng/g,(91.1 ±23.0) ng/g] ,5-HT( (494. 1 ± 50.7) ng/g, (599.7 ± 39.2) ng/g, (541.7 ± 62.6) ng/g) and DA ( ( 298.6 ± 32.6) ng/g, ( 297.0 ± 38.1 ) ng/g, ( 85.9 ± 24.3 ) ng/g) in the high dose of vinpocetine group were significantly higher than that in the normal saline group ( NE (92.4 ± 17.5 ) ng/g, ( 131.4 ± 34.8 ) ng/g, (49.0 ±13.6)ng/g;5-HT(367.8 ±87.3) ng/g,(498.7 ± 79.6) ng/g, (320.4 ±59.4) ng/g; DA( 106.1 ±23.0)ng/g,(97.0 ±21.7)ng/g, (50.4 ± 13.8 )ng/g)(P ＜ 0.01 ). There were increased obviously by the high dose than the low dose of vinpocetine group. Conclusion Vinpocetine could treat PSD by increasing the level of monoamine transmitters in PSD rats' brain.