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Injury in the spinal cord may produce cell death in the brain

DC Field Value Language
dc.contributor.author이배환-
dc.contributor.author김은정-
dc.date.accessioned2015-07-14T16:46:19Z-
dc.date.available2015-07-14T16:46:19Z-
dc.date.issued2004-
dc.identifier.issn0006-8993-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/111557-
dc.description.abstractFunctional deficits after spinal cord injury have originated not only from the direct physical damage itself, but from the secondary biochemical and pathological changes. Apoptotic cell death has been seen around the periphery of an injured site and has been known to ultimately progress to necrosis and infarction. We have initiated the present study focusing on the role of apoptosis in the secondary injury of the brain after acute spinal cord injury (SCI), and conducted a series of experiments, the study examining the morphological changes in the brain following the spinal injury. Under pentobarbital anesthesia, male Sprague–Dawley rats were subjected to SCI model. Rats were laminectomized and SCI was induced using NYU spinal impactor at T9 segment. The behavioral test was performed. Electrophysiologically, motor evoked potentials (MEPs) were recorded. The animals were subjected to morphological study at 12, 24, 48, 72 h, and 1 week, postoperatively. Locomotor deficits were observed after SCI, and changes in the amplitudes and latencies of the MEPs were observed. The morphological changes were evidenced by terminal TUNEL staining and Calbindin-D28K immunohistochemistry. The TUNEL-positive cells were located at the brain motor cortex after SCI. TUNEL-positive cells were seldom found 4 h after injury. In addition, Calbindin-D28K immunoreactive neurons were observed in the motor cortex after injury. These results suggest that apoptosis may play an important role in the pathophysiology of the brain motor cortex following acute spinal cord injury and functions that were deteriorated after SCI may be related to these electrophysiological and morphological changes.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfBRAIN RESEARCH-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHApoptosis*/physiology-
dc.subject.MESHCalbindin 1-
dc.subject.MESHCalbindins-
dc.subject.MESHEvoked Potentials, Motor-
dc.subject.MESHIn Situ Nick-End Labeling-
dc.subject.MESHMale-
dc.subject.MESHMotor Cortex/pathology*-
dc.subject.MESHMotor Neurons/pathology*-
dc.subject.MESHNerve Net/pathology-
dc.subject.MESHNerve Tissue Proteins-
dc.subject.MESHRats-
dc.subject.MESHRats, Sprague-Dawley-
dc.subject.MESHS100 Calcium Binding Protein G/metabolism-
dc.subject.MESHSpinal Cord Injuries/metabolism-
dc.subject.MESHSpinal Cord Injuries/pathology*-
dc.titleInjury in the spinal cord may produce cell death in the brain-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Physiology (생리학)-
dc.contributor.googleauthorBae Hwan Lee-
dc.contributor.googleauthorKyung Hee Lee-
dc.contributor.googleauthorYong Gou Park-
dc.contributor.googleauthorIm-Gap Yi-
dc.contributor.googleauthorSang Sup Choi-
dc.contributor.googleauthorJin-Hun Sohn-
dc.contributor.googleauthorDo Heum Yoon-
dc.contributor.googleauthorUn Jeng Kim-
dc.identifier.doi10.1016/j.brainres.2004.05.113-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.relation.journalcodeJ00392-
dc.identifier.eissn1872-6240-
dc.identifier.pmid15312785-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0006899304008947-
dc.subject.keywordSpinal cord injury-
dc.subject.keywordBrain-
dc.subject.keywordCell death-
dc.subject.keywordBehavior-
dc.subject.keywordCalbindin-
dc.subject.keywordTUNEL-
dc.contributor.alternativeNameLee, Bae Hwan-
dc.rights.accessRightsnot free-
dc.citation.volume1020-
dc.citation.number1-2-
dc.citation.startPage37-
dc.citation.endPage44-
dc.identifier.bibliographicCitationBRAIN RESEARCH, Vol.1020(1-2) : 37-44, 2004-
dc.identifier.rimsid34918-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers

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