ABSTRACT
<p><b>OBJECTIVE</b>To investigate the changes of neural stem cells (NSCs) in the rat hippocampus after cerebral infarction (CI) and to evaluate the neurogenesis caused by the activation of NSCs.</p><p><b>METHODS</b>CI models of rats were made and rats were assigned to 6 groups: sham-operated, 1 day, 3 days, 7 days, 14 days, and 28 days after CI. The dynamic expression of bromodeoxyuridine (BrdU), polysialylated neural cell adhesion molecule (PSA-NCAM), glial fibrillary acidic protein (GFAP), and neuronal nuclear antigen (NeuN) were determined by immunohistochemistry and immunofluorescence staining. BrdU was used to mark the proliferated NSCs. PSA-NCAM was used to mark the plasticity of activated NSCs. GFAP and NeuN were used to mark the differentiated NSCs.</p><p><b>RESULTS</b>Compared with the controls, the number of BrdU+ cells in the hippocampus increased significantly at 1 day after CI (P < 0.05), reached peak at 7 days after CI (P < 0.05), decreased but still elevated compared with the controls at 14 days after CI (P < 0.05), and nearly unchanged at 28 days after CI. The number of BrdU+/PSA-NCAM+ cells increased significantly at 7 days after CI (P < 0.05), reached peak at 14 days after CI (P < 0.05), and decreased but still elevated compared with the controls at 28 days after CI (P < 0.05). The number of BrdU+/PSA-NCAM+ cells was equal to 60% of the number of BrdU+ cells in all the same period. The number of BrdU+/NeuN+ cells in the hippocampus increased significantly at 14 days after CI (P < 0.05) and reached peak at 28 day after CI (P < 0.05). The number of BrdU+/GFAP+ cells in the hippocampus nearly unchanged after CI.</p><p><b>CONCLUSION</b>CI can stimulate the proliferation of inherent NSCs, and most proliferated NSCs may differentiate into neurons and represent neural plasticity.</p>
Subject(s)
Animals , Male , Rats , Adult Stem Cells , Cell Biology , Metabolism , Bromodeoxyuridine , Metabolism , Cell Nucleus , Pathology , Cerebral Infarction , Metabolism , Pathology , Dentate Gyrus , Cell Biology , Metabolism , Glial Fibrillary Acidic Protein , Metabolism , Hippocampus , Cell Biology , Metabolism , Nerve Tissue Proteins , Metabolism , Neural Cell Adhesion Molecule L1 , Metabolism , Neurogenesis , Physiology , Neurons , Cell Biology , Metabolism , Rats, Wistar , Sialic Acids , MetabolismABSTRACT
<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>Compared with controls, the number of BrdU-positive cells in the subventricular zone (SVZ) and hippocampus increased significantly at 1st 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.</p><p><b>CONCLUSION</b>Cerebral infarction may stimulate the proliferation of endogenous neural stem cells in situ and most proliferated neural stem cells represent neural plasticity.</p>
Subject(s)
Animals , Male , Rats , Bromodeoxyuridine , Metabolism , Cell Proliferation , Cerebral Infarction , Metabolism , Pathology , Cerebral Ventricles , Pathology , Hippocampus , Pathology , Neural Cell Adhesion Molecule L1 , Metabolism , Neuronal Plasticity , Neurons , Metabolism , Pathology , Rats, Wistar , Sialic Acids , Metabolism , Stem Cells , Metabolism , PathologyABSTRACT
<p><b>OBJECTIVE</b>To investigate proliferation and differentiation of neural stem cells in adult rats after cerebral infarction.</p><p><b>METHODS</b>Models of cerebral infarction in rats were made and the time-course expression of bromodeoxyuridine (BrdU), Musashi1, glial fibrillary acidic protein (GFAP), and neuronal nuclear antigen (NeuN) were determined by immunohistochemistry and immunofluorescence staining. BrdU and Musashi1 were used to mark dividing neural stem cells. GFAP and NeuN were used to mark differentiating neural stem cells.</p><p><b>RESULTS</b>Compared with controls, the number of BrdU-labeled and BrdU-labeled with Musashi 1-positive cells increased strikingly 1 day after cerebral infarction; approximately 6 fold with a peak 7 days later; markedly decreased 14 days later, but was still elevated compared with that of controls; decling to the control level 28 days later. The number of BrdU-labeled with GFAP-positive cells nearly remained unchanged in the hippocampus after cerebral infarction. The number of BrdU-labeled with NeuN-positive cells increased strikingly 14 days after cerebral infarction, reached maximum peak in the hippocampus 28 days after cerebral infarction in rats.</p><p><b>CONCLUSION</b>Cerebral infarction stimulate proliferation of inherent neural stem cells and most proliferated neural stem cells differentiate into neurons.</p>
