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Dev Neurosci. 2009;31(5):459-70. doi: 10.1159/000232564. Epub 2009 Aug 11.

Astrocytic demise in the developing rat and human brain after hypoxic-ischemic damage.

Author information

1
Département de Neuropathologie, Service d'Anatomie et Cytologie Pathologiques, Hôpital A. Trousseau, Paris, France.

Abstract

In order to approach the physiopathological mechanism underlying the selective susceptibility of the immature brain to hypoxia-ischemia (HI), we have compared the lesions experimentally induced in postnatal day 7 rats using a model of neonatal stroke with those occurring in human fetal and neonatal brains. We first observed that gray and white matter lesions demonstrated a similar organization (core with cell loss and/or cavity and penumbra) and evolutionary pattern between experimental and human HI lesions. We then observed that, in the intermediate white matter, GFAP- and vimentin-positive astrocytes exhibited clasmatodendrosis and represent a major cell population involved in cell death in human brains (56.3 and 67.9%, respectively). In rat brains, GFAP- and TUNEL-positive astrocytes were also highly vulnerable, increasing between 6 (31%) and 72 (58%) hours after ischemia. Together, these results indicate that astroglial dysfunction may play a critical role in determining the progress and outcome of acute hypoxic-ischemic injury particularly in the developing brain.

PMID:
19672074
DOI:
10.1159/000232564
[Indexed for MEDLINE]

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