Objective To investigate whether there is endogenous neural stem cell proliferation and whether these proliferated neural stem cells represent neural plasticity in the adult rats after cerebral infarction.Methods Cerebral infarction models of rats were established and the dynamic expression of bromodeoxyuridine (BrdU), BrdU/polysialylated neural cell adhesion molecule (PSA-NCAM) were determined by immunohistochemistry and immunofluorescence staining. BrdU was used to mark dividing neural stem cells. PSA-NCAM was used to mark the plasticity of neural stem cells.Results Compared with controls, the number of BrdU-positive cells in the subventricular zone (SVZ) and hippocampus increased significantly at 1[KG-*3]st day after cerebral infarction (P<0.05), reached maximum at 7th day, decreased markedly at 14th day, but it was still elevated compared with that of the controls (P<0.05). The number of BrdU-labeled with PSA-NCAM-positive cells increased significantly at 7th day (P<0.05), reached maximum at 14th day, markedly decreased at 28th day, but it was still elevated compared with that of the controls (P<0.05). It was equal to 60% of the number of BrdU-positive cells in the same period.Conclusion Cerebral infarction may stimulate the proliferation of endogenous neural stem cells in situ and most proliferated neural stem cells represent neural plasticity. Objective To investigate whether there is endogenous neural stem cell proliferation and whether these proliferated neural stem cells represent neural plasticity in the adult rats after cerebral infarction. Cerebral infarction models of rats were established and the dynamic expression of bromodeoxyuridine (BrdU), BrdU / polysialylated neural cell adhesion molecule (PSA-NCAM) were determined by immunohistochemistry and immunofluorescence staining. BrdU was used to mark the plasticity of neural stem cells. Results Compared with controls, the number of BrdU -positive cells in the subventricular zone (SVZ) and hippocampus increased significantly at 1 [KG- * 3] st day after cerebral infarction (P <0.05), reached maximum at 7th day, decreased markedly at 14th day, but it was still elevated compared with that of the controls (P <0.05). The number of BrdU-labeled with PSA-NCAM-positive cells increased significantly at 7th day (P <0.05), reached maximum was 14th day, markedly decreased at 28th day, but it was still elevated compared with that of the controls (P <0.05). It was equal to 60% of the number of BrdU-positive cells in the same period. Conflux Cerebral infarction may stimulate the proliferation of endogenous neural stem cells in situ and most proliferated neural stem cells represent neural plasticity.