Objectives: To explore the effects of high-intensity intermittent training ( HIT) on the degree of depression, neuronal morphology, and the expreesion of bran-derived neurotrophic factor ( BDNF) in the hippocampal dentate gyrus ( DG) of ischemic hemisphere in rats with post-stroke depreesion (PSD), and to investigate the potential mechanisms. #Methods: 40 male Wistar rats were randomly divided into control group, sham-operation group (Sham), PSD model group, moderate intensity aerobic training group (MIAT) and HIT group (n =8 for each group ). Except the control and Sham group, all other groups were given the middle cerebral arter occlusion ( MCAO ) using the intraluminal thread method, and chronic unpredictable mild strees (CUMS) was applied. After succusful modeling, training programs of diferent intensity were perormed in the MIAT and the HIT group. Rats in the five groups were subjected to behavioral tests ( open field test and tail suspension test)) before and 28 d after training. Nisl staining was used to obsere the morphological changes of neurons in the left hippocampal DG area. The expreesions of BDNF protein were detected by western blotting and immunohistochemistry. Results : After 28 d of training, compared with the other groups, the PSD group's pause time of the central lattice was prolonged ; the immobility time increased in tail suspension test; the expreesion of BDNF decreased in the left hippocampal DG area. The diference was statisticaUy significant ( 8<0.01). Neurons of hippocampal DG neurons were loosely afranged ; cells were miising. Nisl body was lightly stained and even disolved ; the etiological findings in MIAT and HIT rats were revered ; the exprusion of BDNF was elevated. Nisl staining showed that the cells were aaranged neatly ; the layers were dense, and the Nisl body was deeply stained. The changes in HIT group were more significant than that in MIAT group (8 <0.05). Conclusions: Compared with the traditional medium-intensity aerobic training, high-intensity interval training can improve the depression-like behavior in rats with post-stroke depreesion. The potential mechanism might be that HIT increase the neuroplasticity and ex- preesion of BDNF in hippocampal DG area. [ABSTRACT FROM AUTHOR]