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

Authors
 Bae Hwan Lee  ;  Kyung Hee Lee  ;  Yong Gou Park  ;  Im-Gap Yi  ;  Sang Sup Choi  ;  Jin-Hun Sohn  ;  Do Heum Yoon  ;  Un Jeng Kim 
Citation
 BRAIN RESEARCH, Vol.1020(1-2) : 37-44, 2004 
Journal Title
BRAIN RESEARCH
ISSN
 0006-8993 
Issue Date
2004
MeSH
Animals ; Apoptosis*/physiology ; Calbindin 1 ; Calbindins ; Evoked Potentials, Motor ; In Situ Nick-End Labeling ; Male ; Motor Cortex/pathology* ; Motor Neurons/pathology* ; Nerve Net/pathology ; Nerve Tissue Proteins ; Rats ; Rats, Sprague-Dawley ; S100 Calcium Binding Protein G/metabolism ; Spinal Cord Injuries/metabolism ; Spinal Cord Injuries/pathology*
Keywords
Spinal cord injury ; Brain ; Cell death ; Behavior ; Calbindin ; TUNEL
Abstract
Functional 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.
Full Text
http://www.sciencedirect.com/science/article/pii/S0006899304008947
DOI
10.1016/j.brainres.2004.05.113
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
Yonsei Authors
Kim, Un Jeng(김은정) ORCID logo https://orcid.org/0000-0003-0968-0252
Lee, Bae Hwan(이배환) ORCID logo https://orcid.org/0000-0003-4719-9021
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/111557
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