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Glial responses to neonatal hypoxic–ischemic injury in the rat cerebral cortex
Author(s) -
Sizonenko Stéphane V.,
Camm Emily J.,
Dayer Alexandre,
Kiss Jozsef Z.
Publication year - 2008
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2007.08.014
Subject(s) - oligodendrocyte , nestin , neurogenesis , biology , neuroscience , neuroglia , cerebral cortex , glial scar , immunostaining , lesion , myelin , gliogenesis , cortex (anatomy) , microglia , pathology , astrocyte , central nervous system , progenitor cell , immunohistochemistry , medicine , microbiology and biotechnology , inflammation , immunology , neural stem cell , stem cell
Neurogenesis is nearly completed after birth, whereas gliogenic activities remain intense during the postnatal period in the developing rat cortex. These include involution of radial glia, proliferation of astrocytes and oligodendrocytes and myelin formation. Little is known about the effects of hypoxic–ischemic (HI) injury on these critical postnatal processes. Here we explored the glial reactions to mild HI injury of the neonatal rat cerebral cortex at P3. We show that the HI lesion results in disruption of the normal radial glia architecture, which was paralleled by an increase in GFAP immunopositive reactive astrocytes. The morphology of these latter cells and the fact that they were immunolabelled for both nestin and GFAP suggest an accelerated transformation of radial glia into astrocytes. In addition, BrdU/GFAP immunostaining revealed a significant increase of double‐labelled cells indicating an acute proliferation of astrocytes after HI. This enhanced proliferative activity of astrocytes persisted for several weeks. We found an elevated number and increased mitotic activity of both NG2‐positive oligodendrocyte progenitors and RIP‐positive oligodendrocytes after injury. These findings imply that glial responses are central to cortical tissue remodelling following neonatal ischemia and represent a potential target for therapeutic approaches.