Subplate in a rat model of preterm hypoxia-ischemia.

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Version: Final published version
Serval ID
serval:BIB_B84D0E206B9C
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Subplate in a rat model of preterm hypoxia-ischemia.
Journal
Annals of Clinical and Translational Neurology
Author(s)
Okusa C., Oeschger F., Ginet V., Wang W.Z., Hoerder-Suabedissen A., Matsuyama T., Truttmann A.C., Molnár Z.
ISSN-L
2328-9503
Publication state
Published
Issued date
2014
Peer-reviewed
Oui
Volume
1
Number
9
Pages
679-691
Language
english
Notes
Publication types: Journal ArticlePublication Status: ppublish
Abstract
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.
Pubmed
Open Access
Yes
Create date
18/10/2016 15:30
Last modification date
20/08/2019 15:26
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