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Newborn piglets were subjected to 30 minutes of hypoxia (arterial O<jats:sub>2<\/jats:sub> saturation, 30%) and then 7 minutes of airway occlusion (O<jats:sub>2<\/jats:sub> saturation, 5%), producing cardiac arrest, followed by cardiopulmonary resuscitation. Piglets recovered for 24, 48, or 96 hours. At 24 hours, 66% of putaminal neurons were injured, without differing significantly thereafter, but neuronal densities were reduced progressively (21\u201344%). By DNA nick\u2010end labeling, the number of dying putaminal cells per square millimeter was increased maximally at 24 to 48 hours. Glial fibrillary acidic protein\u2013positive cell body densities were reduced 48 to 55% at 24 to 48 hours but then recovered by 96 hours. Early postischemia, subsets of astrocytes had fragmented DNA; later postischemia, subsets of astrocytes proliferated. By immunocytochemistry, glutamate transporter 1 (GLT1) was lost after ischemia in the astroglial compartment but gained in cells appearing as neurons, whereas neuronal excitatory amino acid carrier 1 (EAAC1) dissipated. By immunoblotting, GLT1 and EAAC1 levels were 85% and 45% of control, respectively, at 24 hours of recovery. Thus, astroglial and neuronal injury occurs rapidly in H\u2010I newborn striatum, with early gliodegeneration and glutamate transporter abnormalities possibly contributing to neurodegeneration.<\/jats:p>","DOI":"10.1002\/ana.410420310","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T15:04:16Z","timestamp":1104591856000},"page":"335-348","source":"Crossref","is-referenced-by-count":237,"title":["Hypoxia\u2014ischemia causes abnormalities in glutamate transporters and death of astroglia and neurons in newborn striatum"],"prefix":"10.1002","volume":"42","author":[{"given":"Lee J.","family":"Martin","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ansgar 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