Subplate in a rat model of preterm hypoxia-ischemia.

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Ressource 1Télécharger: BIB_B84D0E206B9C.P001.pdf (1497.42 [Ko])
Etat: Public
Version: Final published version
ID Serval
serval:BIB_B84D0E206B9C
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Subplate in a rat model of preterm hypoxia-ischemia.
Périodique
Annals of Clinical and Translational Neurology
Auteur⸱e⸱s
Okusa C., Oeschger F., Ginet V., Wang W.Z., Hoerder-Suabedissen A., Matsuyama T., Truttmann A.C., Molnár Z.
ISSN-L
2328-9503
Statut éditorial
Publié
Date de publication
2014
Peer-reviewed
Oui
Volume
1
Numéro
9
Pages
679-691
Langue
anglais
Notes
Publication types: Journal ArticlePublication Status: ppublish
Résumé
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
Oui
Création de la notice
18/10/2016 16:30
Dernière modification de la notice
20/08/2019 16:26
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