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Wistar rats (1\u2010day old) were subjected to hypoxia and the periventricular white matter (corpus callosum) was examined for the mRNA and protein expression of hypoxia\u2010inducible factor\u20101\u03b1 (HIF\u20101\u03b1), endothelial, neuronal and inducible nitric oxide synthase (eNOS, nNOS and iNOS), vascular endothelial growth factor (VEGF) and N\u2010methyl\u2010D\u2010aspartate receptor subunit\u20031 (NMDAR1) between 3\u2003h and 14\u2003days after hypoxic exposure by real\u2010time RT\u2010PCR, western blotting and immunohistochemistry. Up\u2010regulated mRNA and protein expression of HIF\u20101\u03b1, VEGF, NMDAR1, eNOS, nNOS and iNOS in corpus callosum was observed in response to hypoxia. NMDAR1 and iNOS expression was found in the activated microglial cells, whereas VEGF was localized to astrocytes. An enzyme immunoassay showed that the VEGF concentration in corpus callosum was significantly higher up to 7\u2003days after hypoxic exposure. NO levels, measured by colorimetric assay, were also significantly higher in hypoxic rats up to 14\u2003days after hypoxic exposure as compared with the controls. A large number of axons undergoing degeneration were observed between 3\u2003h and 7\u2003days after the hypoxic exposure at electron\u2010microscopic level. Our findings point towards the involvement of excitotoxicity, VEGF and NO in periventricular white matter damage in response to hypoxia.<\/jats:p>","DOI":"10.1111\/j.1471-4159.2006.03964.x","type":"journal-article","created":{"date-parts":[[2006,6,19]],"date-time":"2006-06-19T10:26:53Z","timestamp":1150712813000},"page":"1200-1216","source":"Crossref","is-referenced-by-count":94,"title":["Hypoxic damage to the periventricular white matter in neonatal brain: role of vascular endothelial growth factor, nitric oxide and excitotoxicity"],"prefix":"10.1111","volume":"98","author":[{"given":"Charanjit","family":"Kaur","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Viswanathan","family":"Sivakumar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lin Stella","family":"Ang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alamelu","family":"Sundaresan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2006,6,19]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1053\/j.semperi.2004.10.010"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1203\/01.PDR.0000130472.30874.FF"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1750-3639.2004.tb00492.x"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0005-2728(99)00030-4"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(76)90527-3"},{"key":"e_1_2_8_7_1","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4757-6376-8_4"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-200104000-00003"},{"key":"e_1_2_8_9_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00401-004-0864-9"},{"key":"e_1_2_8_10_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.0477-04.2004"},{"key":"e_1_2_8_11_1","doi-asserted-by":"publisher","DOI":"10.1038\/nm723"},{"key":"e_1_2_8_12_1","doi-asserted-by":"publisher","DOI":"10.1002\/mrdd.10007"},{"key":"e_1_2_8_13_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1750-3639.2005.tb00525.x"},{"key":"e_1_2_8_14_1","first-page":"R286","article-title":"Inhibition of inducible nitric oxide synthase ameliorate cerebral ischemic damage","volume":"268","author":"Iadecola C.","year":"1995","journal-title":"Am. 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