title: Neural precursor cells division and migration in neonatal rat brain after ischemic/hypoxic injury.
abstract: Ischemia/hypoxia (I/H) causes severe perinatal brain disorders such as cerebral palsy. The neonatal brain possesses much plasticity, and to enhance new cell production would be an innovative means of therapy for such disorders. In order to elucidate the dynamic changes of neural progenitor cells in the neonatal brain after ischemia, we investigated new cells production in the subventricular zone and subsequent migration of these cells to the injured area. Newly produced cells were confirmed by incorporation of bromodeoxyuridine (BrdU), and attempt for differentiation was investigated by immunohistochemistry for molecular markers of each cellular lineage. In the sham-control brain, there were many BrdU-labeled cells which gradually decreased as the animal becomes older. Many of these cells were oligodendroglial progenitor or microglial cells. Although there were only few neuronal cells labeled for BrdU in the sham-control, they dramatically increased after I/H. They were located at just beneath the subventricular zone where the progenitor cells reside and to the injured area, indicating that newly produced cells migrated to the infarct region and differentiated into neuronal precursor cells in order to compensate the lost neural cells. We found that BrdU-labeled astroglial, oligodendroglial progenitor, and microglial cells were also increased after I/H, suggesting that they also play active roles in recovery. Progenitor cells may have potential for treating perinatal brain disorders.
authors.affiliation: Department of Neurology, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8558, Japan. thayashi@cc.okayama-u.ac.jp
authors.forename: Takeshi
authors.initials: T
authors.lastname: Hayashi
authors.forename: Masanori
authors.initials: M
authors.lastname: Iwai
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Ikeda
authors.forename: Guang
authors.initials: G
authors.lastname: Jin
authors.forename: Kentaro
authors.initials: K
authors.lastname: Deguchi
authors.forename: Shoko
authors.initials: S
authors.lastname: Nagotani
authors.forename: Hanzhe
authors.initials: H
authors.lastname: Zhang
authors.forename: Yoshihide
authors.initials: Y
authors.lastname: Sehara
authors.forename: Isao
authors.initials: I
authors.lastname: Nagano
authors.forename: Mikio
authors.initials: M
authors.lastname: Shoji
authors.forename: Tsuyomu
authors.initials: T
authors.lastname: Ikenoue
authors.forename: Koji
authors.initials: K
authors.lastname: Abe
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000166:cytology / Q000378:metabolism*; D002455:Cell Division / Q000502:physiology*; D002465:Cell Movement / Q000502:physiology*; D004195:Disease Models, Animal; D020925:Hypoxia-Ischemia, Brain / Q000378:metabolism* / Q000473:pathology*; D007150:Immunohistochemistry; D020547:Lateral Ventricles / Q000166:cytology / Q000378:metabolism*; D009457:Neuroglia / Q000166:cytology / Q000378:metabolism; D009474:Neurons / Q000166:cytology / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D020127:Recovery of Function / Q000502:physiology; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism