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[Abstract Title]. - Society for Neuroscience

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National Multiple Sclerosis <strong>Society</strong>, Grant RG3712A1 (V.G.)<br />

<strong>Title</strong>: Hyperoxia causes astrogliosis in the developing brain<br />

Authors: *T. SCHMITZ, L.-J. CHEW, V. GALLO;<br />

Ctr. <strong>for</strong> Neurosci. Res., Children's Natl. Med. Ctr., Washington, DC<br />

<strong>Abstract</strong>: Periventricular white matter damage is a major cause of impaired neurological<br />

development in premature infants. Contributing factors include perinatal infection, inflammation<br />

and hypoxia/ischemia. High oxygen (80%) concentrations have also been shown to cause<br />

oligodendrocyte progenitor cell death and hypomyelination. In many animal models of perinatal<br />

brain damage, the observation of astrocyte activation (astrogliosis) has often been associated<br />

with CNS inflammation and white matter deficiency. The role of astroglial changes in white<br />

matter loss following oxygen exposure however has not been explored and is the focus of this<br />

study. We investigated the effects of high oxygen concentrations on astrocytes both in vivo and<br />

in vitro. In a transgenic mouse line bearing astrocyte-targeted reporter expression (glial fibrillary<br />

acidic protein promoter, GFAP-EGFP), exposure of postnatal day 6 (P6) pups to 48h hyperoxia<br />

decreased myelin basic protein (MBP) expression in subcortical white matter regions when<br />

analyzed by immunocytochemistry and Western blotting after a 4-day recovery in room air at<br />

P12. These observations at P12 were associated with markedly elevated GFAP-EGFP and GFAP<br />

expression levels (P

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