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Minocycline is a potent inhibitor of microglia and may have a role as a neuroprotective agent that ameliorates brain injury after hypoxia\u2013ischemia in neonatal animal models. However to date large doses, pre\u2010insult administration and short periods of treatment after hypoxia\u2013ischemia have mostly been investigated in animal models making it difficult to translate minocycline's potential applicability to protect the human preterm neonatal brain exposed to hypoxia\u2013ischemia. We investigated whether repeated doses of minocycline can minimize white matter injury and neuroinflammation one week after hypoxia\u2013ischemia (right carotid artery ligation and 30 min 6% O<jats:sub>2<\/jats:sub>) in the post\u2010natal day 3 rat pup. Two dosage regimens of minocycline were administered for one week; a high dose of 45 mg\/kg 2 h after hypoxia\u2013ischemia then 22.5 mg\/kg daily or a low dose 22.5 mg\/kg 2 h after hypoxia\u2013ischemia then 10 mg\/kg. Post\u2010natal day 3 hypoxia\u2013ischemia significantly reduced myelin content, numbers of O1\u2010 and O4\u2010positive oligodendrocyte progenitor cells and increased activated microglia one week later on post\u2010natal day 10. The low dose minocycline regimen was as effective as the high dose in ameliorating neuroinflammation after post\u2010natal day 3 hypoxia\u2013ischemia. However only the high dose regimen significantly attenuated reductions in O1\u2010 and O4\u2010positive oligodendrocyte progenitor cells and myelin content. The low dose only significantly attenuated the reduction in O1\u2010positive oligodendrocyte cell counts. Repeated, daily, post\u2010insult treatment with minocycline abolished neuroinflammation and may provide neuroprotection to white matter for up to one week after hypoxia\u2013ischemia in a rodent preterm model. The present findings suggest the potential clinical relevance of a repeated, daily minocycline treatment strategy, administered after a hypoxia\u2013ischemia insult, as a therapeutic intervention for hypoxia\u2013ischemia\u2010affected preterm neonates.<\/jats:p><\/jats:sec>","DOI":"10.1016\/j.ijdevneu.2008.02.005","type":"journal-article","created":{"date-parts":[[2008,3,5]],"date-time":"2008-03-05T19:11:51Z","timestamp":1204744311000},"page":"477-485","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":93,"title":["Post\u2010insult minocycline treatment attenuates hypoxia\u2010ischemia\u2010induced neuroinflammation and white matter injury in the neonatal rat: a comparison of two different dose regimens"],"prefix":"10.1002","volume":"26","author":[{"given":"Michelle L.","family":"Carty","sequence":"first","affiliation":[{"name":"Perinatal Research Centre School of Medicine, University of Queensland Herston Queensland 4029 Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie A.","family":"Wixey","sequence":"additional","affiliation":[{"name":"Perinatal Research Centre School of Medicine, University of Queensland Herston Queensland 4029 Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul B.","family":"Colditz","sequence":"additional","affiliation":[{"name":"Perinatal Research Centre School of Medicine, University of Queensland Herston Queensland 4029 Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kathryn M.","family":"Buller","sequence":"additional","affiliation":[{"name":"Perinatal Research Centre School of Medicine, University of Queensland Herston Queensland 4029 Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2008,3,4]]},"reference":[{"key":"e_1_2_4_2_1","doi-asserted-by":"publisher","DOI":"10.1159\/000103741"},{"key":"e_1_2_4_3_1","doi-asserted-by":"publisher","DOI":"10.1001\/jama.289.24.3264"},{"key":"e_1_2_4_4_1","doi-asserted-by":"publisher","DOI":"10.1002\/ana.10242"},{"key":"e_1_2_4_5_1","doi-asserted-by":"crossref","first-page":"6241","DOI":"10.1523\/JNEUROSCI.18-16-06241.1998","article-title":"Maturation\u2010dependent vulnerability of oligodendrocytes top oxidative stress\u2010induced death caused by glutathione depletion","volume":"18","author":"Back S.A.","year":"1998","journal-title":"J. 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