title: Immature and mature neurons coexist among glial scars after rat traumatic brain injury.
abstract: OBJECTIVE
  Glial scars around a damaged area after brain injury inhibit neurite elongation from surviving neurons and axonal plasticity, and thus prevent neural network regeneration. However, the generation, differentiation and maturation of neural stem cells (NSCs) among glial scars after brain injury have not yet been reported.
  
  
  METHODS
  In the present study, we investigated the chronological relationship between gliosis and maturation of new neurons around a damaged area using a rat traumatic brain injury (TBI) model.
  
  
  RESULTS
  Between 1 and 7 days after injury, many nestin-positive cells were observed around the damaged area. Three days after injury, many small nestin-positive cells showed an astrocytic morphology. Between 1 and 30 days after injury, doublecortin (DCX)-positive cells were present around the damaged area. Three and 7 days after injury, a small number of nestin-positive cells were immunopositive for glial fibrillary acidic protein (GFAP). Seven days after injury, there were DCX-positive cells in the gliosis occurring in the lesion. Thirty days after injury, DCX-positive cells were observed near and among the glial scars and a small number of these cells were immunopositive for NeuN.
  
  
  CONCLUSIONS
  These results suggest that DCX-positive cells were present near and among the glial scars after brain injury, and that these cells changed from immature to mature neurons. It is considered that promotion of the maturation and differentiation of newly formed immature neurons near and among glial scars after injury may improve the brain dysfunction induced by glial scars after brain injury.
authors.affiliation: Department of Pathology, Kinki University School of Medicine, Osaka, Japan. tatsuki@med.kindai.ac.jp
authors.forename: Tatsuki
authors.initials: T
authors.lastname: Itoh
authors.forename: Takao
authors.initials: T
authors.lastname: Satou
authors.forename: Shozo
authors.initials: S
authors.lastname: Nishida
authors.forename: Shigeo
authors.initials: S
authors.lastname: Hashimoto
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Ito
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000166:cytology / Q000378:metabolism; D015415:Biomarkers / Q000032:analysis / Q000378:metabolism; D001930:Brain Injuries / Q000150:complications* / Q000473:pathology / Q000503:physiopathology*; D002454:Cell Differentiation; D002921:Cicatrix / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D000089622:Doublecortin Domain Proteins; D000089662:Doublecortin Protein; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology*; D007150:Immunohistochemistry; D007381:Intermediate Filament Proteins / Q000378:metabolism; D008297:Male; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D009416:Nerve Regeneration; D009419:Nerve Tissue Proteins / Q000378:metabolism; D064231:Nestin; D009474:Neurons / Q000166:cytology / Q000378:metabolism*; D009479:Neuropeptides / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism
chemical_list: D015415:Biomarkers; C000714848:Dcx protein, rat; D000089622:Doublecortin Domain Proteins; D000089662:Doublecortin Protein; D005904:Glial Fibrillary Acidic Protein; D007381:Intermediate Filament Proteins; D008869:Microtubule-Associated Proteins; D009419:Nerve Tissue Proteins; C577486:Nes protein, rat; D064231:Nestin; D009479:Neuropeptides