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Models Of Spinal Cord Injury In Rats And Primary Study Of Glial Scar

Posted on:2004-11-05Degree:MasterType:Thesis
Country:ChinaCandidate:Y P YangFull Text:PDF
GTID:2144360095961348Subject:Surgery
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Objects: Spinal cord injury(SCI) is the main reason for paraplegia, but the effective therapies to it is very poor. Traditionally, the adult CNS environment is restrictive to axonal regeneration. In recent years it has been demonstrated that injuried CNS axons are capable of growth when their environment is manipulated. But it is maintained that regeneration failure following injury is due primarily to a structural barrier to axon growth, the so-called "glial scar". In order to study the glial scar mechanism, the models of SCI were established in the rats. The spinal cord function, evoked potentials and pathological changes after SCI were regularly observed. Methods: 46 adult Sprague-Dawley rats (weight 200-250g) of either sex were divided randomly into severe SCI group(n=20), moderate SCI group(n=20) and control SCI group(n=6). All animals were anesthetized with amobarbital sodium(100mg/Kg) and SCI lesions were made at T10 segment of spine with modified Allen's impact device. The severe group and moderate group were contused by 300gcf(30g×10cm) and 150gcf(30g×5cm) energy respectively. The control group only accepted the pseudo- operation. Locomotor capacity was assessed according to the 21-point Basso, Beattie and Bresnahan score; Both SEP and MEP were recorded by the dignostic EMG/EP/IOM system(KEYPOINT-4). The lesions were observed with light microscopy and electron microscopy(EM) at 1w, 2w and 8w after SCI. The GFAP and vimentin were also observed with immunohistochemistry(IHC) .Result: The mortality rate of severe SCI group and moderate SCI group was 35% and 20% respectively. The BBB scores of severe group were 0, 1.79±0.70, 3.50±1.51, 4.31±2.32, 4.77±2.39, 5.15±3.21 at 1d, 1w, 2w, 4w, 6w, and 8w. The BBB scores of moderate group were 1.70±2.13, 6.00±3.40, 10.32±3.40, 11.28±3.39, 13.43±3.74, 14.06±3.57 at 1d, 1w, 2w, 4w, 6w, and 8w. The latency and amplitude of SEP and MEP in severe group were obviously delayed and decreased until 8w after SCI. The latency and amplitude of SEP and MEP in moderate group were also delayed and decreased, partically improved at 8w after SCI. There were cysts in glial scars at injuried lesion at 8w in two groups and the sizes of them were larger in the severe group than in the moderate group.Hemorrhage and necrosis could be seen at the early stage. Myelin collapsing and astrocyte degeneration were found at 2w. Astrocyte hyperplasia were found at 8w after SCI. The expression of GFAP and vimentin were found obviously at 2w after injury. The cyst with glial scar around it was the prominent pathological changes at the same position during 8w after injury. Concusions: The models produced by modified Allen's impact device are useful to the study of SCI. SEP and MEP can reflect the degree of SCI objectively and confidently. The size of glial scar might inhibit the functional recovery after SCI. The GFAP and vimentin are good markers of the morphological range of glial scar.
Keywords/Search Tags:spinal cord injury(SCI), somatosensory evoked potential(SEP), motor evoked potential(MEP) glial fibrillary acidic protein(GFAP) Vimentin(Vim), animal model
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