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dc.contributor.authorCengiz, Pelin
dc.contributor.authorAKTURE, Erinc
dc.contributor.authorHUTCHINSON, Elizabeth
dc.contributor.authorSONG, Chihwa
dc.contributor.authorKendigelen, Pınar
dc.contributor.authorBUDOFF, Greg E.
dc.contributor.authorLEE, Jihae
dc.contributor.authorFERRAZZANO, Peter
dc.contributor.authorSUN, Dandan
dc.contributor.authorMEYERAND, Elizabeth
dc.contributor.authorZHANG, Louise
dc.contributor.authorULUC, Kutluay
dc.date.accessioned2021-03-05T13:54:59Z
dc.date.available2021-03-05T13:54:59Z
dc.identifier.citationCengiz P., ULUC K., Kendigelen P., AKTURE E., HUTCHINSON E., SONG C., ZHANG L., LEE J., BUDOFF G. E. , MEYERAND E., et al., "Chronic Neurological Deficits in Mice after Perinatal Hypoxia and Ischemia Correlate with Hemispheric Tissue Loss and White Matter Injury Detected by MRI", DEVELOPMENTAL NEUROSCIENCE, cilt.33, ss.270-279, 2011
dc.identifier.issn0378-5866
dc.identifier.otherav_b487d5f5-aebe-4459-873c-6cc347dc87de
dc.identifier.othervv_1032021
dc.identifier.urihttp://hdl.handle.net/20.500.12627/120216
dc.identifier.urihttps://doi.org/10.1159/000328430
dc.description.abstractWe investigated the effects of perinatal hypoxia-ischemia (HI) on brain injury and neurological functional outcome at postnatal day (P) 30 through P90. HI was induced by exposing P9 mice to 8% O-2 for 55 min using the Vannucci HI model. Following HI, mice were treated with either vehicle control or Na+/H+ exchanger isoform 1 (NHE1) inhibitor HOE 642. The animals were examined by the accelerating rotarod test at P30 and the Morris water maze (MWM) test at P60. T-2-weighted MRI was conducted at P90. Diffusion tensor imaging (DTI) was subsequently performed in ex vivo brains, followed by immunohistochemical staining for changes in myelin basic protein (MBP) and neurofilament protein expression in the corpus callosum (CC). Animals at P30 after HI showed deficits in motor and spatial learning. T-2 MRI detected a wide spectrum of brain injury in these animals. A positive linear correlation was observed between learning deficits and the degree of tissue loss in the ipsilateral hemisphere and hippocampus. Additionally, CC DTI fractional anisotropy (FA) values correlated with MBP expression. Both FA and MBP values correlated with performance on the MWM test. HOE 642-treated mice exhibited improved spatial learning and memory, and less white matter injury in the CC. These findings suggest that HI-induced cerebral atrophy and CC injury contribute to the development of deficits in learning and memory, and that inhibition of NHE1 is neuroprotective in part by reducing white matter injury. T-2-weighted MRI and DTI are useful indicators of functional outcome after perinatal HI. Copyright (C) 2011 S. Karger AG, Basel
dc.language.isoeng
dc.subjectYaşam Bilimleri
dc.subjectMoleküler Biyoloji ve Genetik
dc.subjectMikrobiyal Genetik
dc.subjectTemel Bilimler
dc.subjectGELİŞİMSEL BİYOLOJİ
dc.subjectMoleküler Biyoloji ve Genetik
dc.subjectYaşam Bilimleri (LIFE)
dc.subjectNEUROSCIENCES
dc.subjectSinirbilim ve Davranış
dc.titleChronic Neurological Deficits in Mice after Perinatal Hypoxia and Ischemia Correlate with Hemispheric Tissue Loss and White Matter Injury Detected by MRI
dc.typeMakale
dc.relation.journalDEVELOPMENTAL NEUROSCIENCE
dc.contributor.departmentUniversity of Wisconsin System , ,
dc.identifier.volume33
dc.identifier.startpage270
dc.identifier.endpage279
dc.contributor.firstauthorID98277


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