{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T21:20:46Z","timestamp":1790889646405,"version":"4.1.0"},"reference-count":46,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2004,3,10]],"date-time":"2004-03-10T00:00:00Z","timestamp":1078876800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Glia"],"published-print":{"date-parts":[[2004,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Neonatal hypoxic\u2010ischemic (HI) white matter injury is a major contributor to chronic neurological dysfunction. Immature oligodendrocytes (OLGs) are highly vulnerable to HI injury. As little is known about in vivo OLG repair mechanisms in neonates, we studied whether new OLGs are generated after HI injury in P7 rats. Rats received daily BrdU injections at P12\u201314 or P21\u201322 and sacrificed at P14 to study the level of cell proliferation or at P35 to permit dividing OLG precursors to differentiate. In P14 HI\u2010injured animals, the number of BrdU<jats:sup>+<\/jats:sup> cells in the injured hemisphere is consistently greater than controls. At P35, sections were double\u2010labeled for BrdU and markers for OLGs, astrocytes, and microglia. Double\u2010labeled BrdU<jats:sup>+<\/jats:sup>\/myelin basic protein<jats:sup>+<\/jats:sup> and BrdU<jats:sup>+<\/jats:sup>\/carbonic anhydrase<jats:sup>+<\/jats:sup> OLGs are abundant in the injured striatum, corpus callosum, and the infarct core. Quantitative studies show four times as many OLGs are generated from P21\u201335 in HI corpora callosa than controls. Surprisingly, the infarct core contains many newly generated OLGs in addition to hypertrophied astrocytes and activated microglia. These glia and non\u2010CNS cells may stimulate OLG progenitor proliferation or induce their migration. At P35, astrogliosis and microgliosis are dramatic ipsilaterally but only a few microglia and some astrocytes are BrdU<jats:sup>+<\/jats:sup>. This finding indicates microglial and astrocytic hyperplasia occurs shortly after HI but before the P21 BrdU injections. Although the neonatal brain undergoes massive cell death and atrophy the first week after injury, it retains the potential to generate new OLGs up to 4 weeks after injury within and surrounding the infarct. \u00a9 2004 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/glia.20013","type":"journal-article","created":{"date-parts":[[2004,4,6]],"date-time":"2004-04-06T20:05:03Z","timestamp":1081281903000},"page":"380-390","source":"Crossref","is-referenced-by-count":90,"title":["New oligodendrocytes are generated after neonatal hypoxic\u2010ischemic brain injury in rodents"],"prefix":"10.1002","volume":"46","author":[{"given":"Aliya U.","family":"Zaidi","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Denise A.","family":"Bessert","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennifer 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