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.
Original language | English (US) |
---|---|
Pages (from-to) | 459-70 |
Number of pages | 12 |
Journal | Developmental Neuroscience |
Volume | 31 |
Issue number | 5 |
DOIs | |
State | Published - 2009 |
Keywords
- Animals
- Animals, Newborn
- Apoptosis
- Astrocytes
- Brain
- Cell Count
- Female
- Fetus
- Glial Fibrillary Acidic Protein
- Humans
- Hypoxia-Ischemia, Brain
- Immunohistochemistry
- In Situ Nick-End Labeling
- Male
- Neurons
- Rats
- Staining and Labeling
- Vimentin
- Journal Article