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The specific phase of the oligodendroglial lineage affected has been defined from study of both human brain and experimental models. This premyelinating cell (pre\u2010OL) is vulnerable because of a series of maturation\u2010dependent events. The pathogenesis of pre\u2010OL injury relates to operation of two upstream mechanisms, hypoxia\u2010ischemia and systemic infection\/inflammation, both of which are common occurrences in premature infants. The focus of this review and of our research over the past 15\u201320 years has been the cellular and molecular bases for the maturation\u2010dependent vulnerability of the pre\u2010OL to the action of the two upstream mechanisms. Three downstream mechanisms have been identified, i.e., microglial activation, excitotoxicity and free radical attack. The work in both experimental models and human brain has identified a remarkable confluence of maturation\u2010dependent factors that render the pre\u2010OL so exquisitely vulnerable to these downstream mechanisms. Most importantly, elucidation of these factors has led to delineation of a series of potential therapeutic interventions, which in experimental models show marked protective properties. The critical next step, i.e., clinical trials in the living infant, is now on the horizon.<\/jats:p>","DOI":"10.1016\/j.ijdevneu.2011.02.012","type":"journal-article","created":{"date-parts":[[2011,3,7]],"date-time":"2011-03-07T23:21:35Z","timestamp":1299540095000},"page":"423-440","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":336,"title":["The developing oligodendrocyte: key cellular target in brain injury in the premature infant"],"prefix":"10.1002","volume":"29","author":[{"given":"Joseph J.","family":"Volpe","sequence":"first","affiliation":[{"name":"Department of Neurology Children's Hospital and Harvard Medical School Boston MA 02115 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hannah C.","family":"Kinney","sequence":"additional","affiliation":[{"name":"Department of Pathology Children's Hospital and Harvard Medical School Boston MA 02115 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frances E.","family":"Jensen","sequence":"additional","affiliation":[{"name":"Department of Neurology Children's Hospital and Harvard Medical School Boston MA 02115 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul A.","family":"Rosenberg","sequence":"additional","affiliation":[{"name":"Department of Neurology Children's Hospital and Harvard Medical School Boston MA 02115 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2011,3,5]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1542\/peds.2008-2816"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1460-9568.1996.tb01278.x"},{"key":"e_1_2_8_4_1","doi-asserted-by":"crossref","first-page":"234","DOI":"10.1006\/nbdi.2001.0457","article-title":"Ca(2+) influx through AMPA or kainate receptors alone is sufficient to initiate excitotoxicity in cultured oligodendrocytes","volume":"2","author":"Alberdi E.","year":"2002","journal-title":"Neurobiol. 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