title: Neurogenesis by activation of inherent neural stem cells in the rat hippocampus after cerebral infarction.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  CI can stimulate the proliferation of inherent NSCs, and most proliferated NSCs may differentiate into neurons and represent neural plasticity.
authors.affiliation: Department of Neurosurgery, the First Affiliated Hospital of Dalian Medical University, Dalian 116011, China. zhangbodl@126.com
authors.forename: Bo
authors.initials: B
authors.lastname: Zhang
authors.forename: Ren-zhi
authors.initials: RZ
authors.lastname: Wang
authors.forename: Zhi-gang
authors.initials: ZG
authors.lastname: Lian
authors.forename: Yang
authors.initials: Y
authors.lastname: Song
authors.forename: Yong
authors.initials: Y
authors.lastname: Yao
mesh_terms: D053687:Adult Stem Cells / Q000166:cytology* / Q000378:metabolism; D000818:Animals; D001973:Bromodeoxyuridine / Q000378:metabolism; D002467:Cell Nucleus / Q000473:pathology; D002544:Cerebral Infarction / Q000378:metabolism / Q000473:pathology*; D018891:Dentate Gyrus / Q000166:cytology / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006624:Hippocampus / Q000166:cytology* / Q000378:metabolism; D008297:Male; D009419:Nerve Tissue Proteins / Q000378:metabolism; D039842:Neural Cell Adhesion Molecule L1 / Q000378:metabolism; D055495:Neurogenesis / Q000502:physiology*; D009474:Neurons / Q000166:cytology* / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012794:Sialic Acids / Q000378:metabolism
chemical_list: D005904:Glial Fibrillary Acidic Protein; D009419:Nerve Tissue Proteins; D039842:Neural Cell Adhesion Molecule L1; D012794:Sialic Acids; C103469:polysialyl neural cell adhesion molecule; D001973:Bromodeoxyuridine