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Subplate in a rat model of preterm hypoxia-ischemia.
Journal article

Subplate in a rat model of preterm hypoxia-ischemia.

  • Okusa C Department of Physiology, Anatomy and Genetics, University of Oxford Oxford, United Kingdom ; Institute for Advanced Medical Sciences, Hyogo College of Medicine Hyogo, Japan.
  • Oeschger F Department of Physiology, Anatomy and Genetics, University of Oxford Oxford, United Kingdom.
  • Ginet V Division of Neonatology, Department of Pediatrics, University Hospital Center and University of Lausanne Lausanne, Switzerland.
  • Wang WZ Department of Physiology, Anatomy and Genetics, University of Oxford Oxford, United Kingdom.
  • Hoerder-Suabedissen A Department of Physiology, Anatomy and Genetics, University of Oxford Oxford, United Kingdom.
  • Matsuyama T Institute for Advanced Medical Sciences, Hyogo College of Medicine Hyogo, Japan.
  • Truttmann AC Division of Neonatology, Department of Pediatrics, University Hospital Center and University of Lausanne Lausanne, Switzerland.
  • Molnár Z Department of Physiology, Anatomy and Genetics, University of Oxford Oxford, United Kingdom.
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  • 2014-12-11
Published in:
  • Annals of clinical and translational neurology. - 2014
English OBJECTIVE
Hypoxia-ischemia (HI) in preterm infants primarily leads to injuries in the cerebral white matter. However, there is growing evidence that perinatal injury in preterms can also involve other zones including the cortical gray matter. In a neonatal rat model of HI, selective vulnerability of subplate has been suggested using BrdU birth-dating methods. In this study, we aimed to investigate the neuropathological changes of the subplate and deep layers of the cortex following cerebral HI in neonatal rats with specific cell markers.


METHODS
P2 rats underwent permanent occlusion of the right common carotid artery followed by a period of hypoxia. P8 rats were analyzed using immunohistochemistry; subplate and deep layers cells were quantified and compared with sham-operated case.


RESULTS
A large variability in the extent of the cerebral injury was apparent. For the three analyzed subplate populations (Nurr1+, Cplx3+, and Ctgf+ cells), no significant cell reduction was observed in mild and moderate cases. Only in severe cases, subplate cells were strongly affected, but these injuries were always accompanied by the cell reductions in layers VI and V.


INTERPRETATION
We could therefore not confirm a specific vulnerability of subplate cells compared to other deep layers or the white matter in our model.
Language
  • English
Open access status
gold
Identifiers
Persistent URL
https://sonar.ch/global/documents/19266
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