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实验性自身免疫性脑脊髓炎神经细胞内钙离子的变化及其意义 被引量:1

Study on the Change of the Intracellular Ca^(2+)in Neural Cells in Experimental Autoimmune Encephalomyelitis and Its Significance
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摘要 目的探讨实验性自身免疫性脑脊髓炎(experimentalautoimmuneencephalomyelitis,EAE)发病初期及高峰期活体脑片内Ca2+荧光强度的变化,明确神经细胞内Ca2+的变化与病情演变的关系。方法采用激光共聚焦扫描显微镜(laserscanconfocalmicroscope,LSCM)对荧光探剂fluo3/AM负载的活体脑片进行观察,比较EAE发病初期组、高峰期组及正常对照组小鼠脑片的皮层、实质区域Ca2+的相对荧光强度。结果EAE发病初期组及空白对照组小鼠大脑皮层的Ca2+荧光强度均明显高于脑实质部位(P<0.05)、EAE高峰期组大脑皮层及脑内局灶区域的Ca2+相对荧光强度高于EAE初发病组(P<0.05)。结论EAE小鼠大脑皮层及脑内局灶区域均存在着神经细胞内的Ca2+内流,这种改变随着EAE病情的进展而增强。 Objective To explore the change of Ca^(2+) fluorescence intensity in brain slices at the onset and the peak of Experimental Autoimmune Encephalomyelitis and determine the relationship between it and the progression of this disease. Method The brain slices loaded with fluo-3/AM were observed using laser confocal scanning microscope and the relative Ca^(2+) fluorescence intensity in cortices and parenchyma was compared between the gronps of the onset and the peak of EAE,and the control goup.Results Ca^(2+) fluorescence intensity on the cortices of brain slices is higher than that in parenchyma at the onset of EAE and in the controls. Ca^(2+) fluorescence intensity at the peak of EAE is significantly higher than that at the onset on cortices and the local area of parenchyma.Conclusions In EAE mice there is obvious influx of Ca^(2+) in neural cells in the cortices and the local area in parenchyma and its increase is accompanied with the progression of EAE.
出处 《苏州大学学报(医学版)》 CAS 北大核心 2005年第3期358-361,365,共5页 Suzhou University Journal of Medical Science
基金 江苏省卫生厅重大课题(H200302)
关键词 EAE 激光共聚焦显微镜 Ca^(2+)荧光强度 EAE laser scan confocal microscope Ca^(2+)fluorescence intensity
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  • 1Peter Rieckmann, Mathias Maurer. Anti-inflammatory strategies to prevent axonal injury in mutiple sclerosis[J]. Current opinion in Neurology, 2002,15:361-370.
  • 2邢虹,何其华,袁兰,徐家,吴本.局灶性脑缺血再灌损伤时神经细胞内Ca^(2+)时空动态变化的实验研究[J].中国组织化学与细胞化学杂志,1999,8(1):51-56. 被引量:11
  • 3Hooper D C, Scott G S, Zborek A, et al. Uric acid, a peroxynitrite scavenger, inhibits CNS inflammation, blood-CNS barrier permeability changes, and tissue damage in a mouse model of multiple sclerosis[J]. FASEBJ, 2000,14:691-698.
  • 4Rhonda R Voskuhl. Chronic Relapsing experimental allergic encephalomyelitis in the SJL Mouse: relevant techniques[J]. METHODS: A Companion to Methods in Enzymology, 1996,10(3):435-439.
  • 5Raine CS. Demyelinating diseases, In: Davis RL, Robertson DM, editors. Textbook of Neuropathology [M]. 3^rd ed. New York: Williams and Wilkins, 1997:627-714.
  • 6Antel J. Mutiple sclerosis-emerging concepts of disease pathogenesis[Review][J]. J Neuroimmunol, 1999, 98:45-48.
  • 7Bjartmar C, Trapp BD. Axonal damage and neuronal degeneration in multiple sclerosis:mechanisms and functional consequences[Review] [J]. Curr Opin Neurol, 2001,14:271-278.
  • 8Bjartmar C, Kinkel RP, Kidd G, et al. Axonal loss in normal-appearing white matter in a patient with acute MS[J]. Neurology, 2001,57:1248-1252.
  • 9Smith T, Groom A, Zhu B, et al. Autoimmune encephalomyelitis ameliorated by AMPA antagonists[J].Nat Med, 2000,6:62-64.
  • 10Peterson JW, Bo L, Mork S, et al. Trapp BD. Transected neurites, apoptotic neurons and reduced inflammation in cortical multiple sclerosis lesions[J]. Ann Neurol, 2001,50:389-400.

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