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难治性癫痫患者颞叶新皮质中NCAM-140kDa的表达:颞叶新皮质的可塑性与难治性癫痫的关系 被引量：2

The expression of NCAM-140kDa in temporal lobe neocortex of patients with intractable epilepsy:the relation between the plasticity of temporal lobe neocortex and intractable epilepsy
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摘要 目的研究难治性颞叶癫痫患者颞叶新皮质中NCAM-140kDa(神经细胞粘附分子B)的表达,探讨其在难治性癫痫形成中的意义,并初步探讨颞叶新皮质的可塑性与难治性癫痫的关系。方法按随机化原则,在我们建立的难治性癫痫患者术后脑组织库中抽取15例患者的颞叶脑组织,用免疫组织化学、免疫荧光法分别检测其NCAM-140kDa的表达,并与对照组进行比较。结果免疫组化检测到的实验组和对照组的NCAM-140kDa平均光密度值分别为:0.2290±0.0427、0.1789±0.0258,两组比较差异有显著性(P<0.05)。免疫荧光检测到的实验组和对照组的NCAM荧光强度分别为28.8345±3.2635、20.4513±2.2834,与对照组相比,差异有显著性(P<0.05)。结论NCAM-140kDa在难治性颞叶癫痫患者的颞叶新皮质中表达增加,提示其参与了难治性颞叶癫痫的形成及颞叶皮质神经细胞的可塑性改变与难治性癫痫的形成密切相关。 Objective To investigate the expression of NCAM-140kDa in the temporal lobe neocortex of patients with intractable temporal lobe epilepsy and discuss its roles in the formation of intractable epilepsy. Methods 20 cases of brain tissues of intractable epilepsy and 15 cases of nonepileptic brain tissues were collected. The expression of NCAM- 140kDa in the specimens were examined through immunohistochemistry and indirect immunofluorescence. Results The NCAM-140kDa staining intensity of immunohistochemistry in the intractable epileptic temporal lobe tissue and the control were 0. 2290 ± 0. 0427 and 0. 1789 ±0. 0258, respectively （ P 〈 0. 05 ）, and the intensity of immunofluorescence were 28.8345 ±3.2635 and 20.4513 ±2.2834,respectively（P 〈0.05）. Conclusion The expression of NCAM-140kDa has a significant increase in the intractable epileptic temporal lobe neocortex, suggest it might be involved in the formation of intractable epilepsy, and the changes of plasticity of neurons in temporal lobe is closely related with the formation of intractable epilepsy.
作者 林涛 王学峰 曾艳 李劲梅 席志芹 肖飞
机构地区 重庆医科大学第一附属医院
出处 《中风与神经疾病杂志》 CAS CSCD 北大核心 2008年第3期305-308,共4页 Journal of Apoplexy and Nervous Diseases
关键词 难治性癫痫 NCAM-140kDa 免疫组化 免疫荧光 可塑性 Intractable epilepsy NCAM-140kDa Immunohistochemistry Immunofluorescence Plasticity
分类号 R742.1 [医药卫生—神经病学与精神病学]
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参考文献24

  • 1Ronn LC, Hartz BP, Bock E. The neural cell adhesion molecule (NCAM) in development and plasticity of the nervous system [ J ]. Exp Gerontol, 1998,33:853-864.
  • 2Ronn LC, Berezin V, Bock E. The neural cell adhesion molecule in synaptic plasticity and ageing [ J ]. J Dev Neurosci, 2000,18 : 193- 199.
  • 3Berezin V ,Bock E, Poulsen FM. The neural cell adhesion molecule [ J ]. Curt Opin Drug Disc Dev,2000,3:605-609.
  • 4Li HN, Decreased expression of thyroid receptor-associated protein220 [ J ]. Biochemical and Biophysical Research Communications,2006,8 : 10.
  • 5王学峰,肖波,孙红斌.耐药性癫痫[M].上海科学技术出版社,2002.27-30.
  • 6Leite JP, Neder L, Arisi GM, et al. Plasticity, synaptic strength, and epilepsy : what can we learn from ultrastruetural data [ J ] ? Epilepsia, 2005,46(5 ) : 134-41.
  • 7Scharfman E. Epilepsy as an Example of Neural Plasticity [ J ]. The Neuroscientist ,2002,8 (2) : 154-173.
  • 8Emilio R, Sanabria G. Damage, Reorganization, and Abnormal Neocortical Hyperexcitability in the Pilocarpine Model of Temporal Lobe Epilepsy [ J ]. Epilepsia ,2002,43 ( 5 ) : 96-106.
  • 9Chen IS, Wang JG, Baneqee PK, et al. Kainic acid induced focal cortical seizure is associated with an increase of synaptophysin immunoreactivity in the cortex[ J ]. Exp Neurol, 1996,141:25-31.
  • 10DeFelipe OJ. The neuropathology of temporal lobe epilepsy : primary and secondary changes in the cortical circuits and epileptogenicity [ J ]. Rev Neurol,2002,34 (5) :401-408.

二级参考文献10

  • 1Gentleman SM, Nash M J, Sweeting C J, et al. β -Amyloid precursor protein (βAPP) as a marker for axonal injury after head injury.Neurosci Lett, 1993, 160: 139-144.
  • 2Li Gui Lin, Mohammad F, Olsson Y, et al. Changes of β -amyloid precursor protein after compression trauma to the spinal cord: An experimental study in the rat using immunohistochemistry. J Neurotrauma,1995, 12: 269-277.
  • 3Ahlgren S, Li Gui Lin, Olsson Y, et al. Accumulation of β-Amyloid precursor protein and ubiquitin in axons after spinal cord trauma in humans: immunohistochemical observations on autopsy material.Acta Neuropathol, 1996, 92:49-55
  • 4Bergmann M, Lahr G, Mayerhofer A, et al. Expression of synaptophysin during the prenatal development of the rat spinal cord: correlation with basic differentiation processes of neurons. Neurosci, 1991, 42: 569-582.
  • 5Eastwood SL, Burnet PW, McDonald B, et al. Synaptophysin gene expression in human brain: a quantitative in situ hybridization and immunohistochemical study. Neurosci, 1994, 59: 881-892.
  • 6Chen LS, Wong JG, Banerjee PK, et al. Kainic acid-induced focal cortical seizure is associated with an increase of synaptophysin immunoreactivity in the cortex. Exp Neurol, 1996, 141: 25-31.
  • 7Li Gui Lin, Tan YL, Wang YC, et al. Spike waves and synaptic ultrastructure in human epileptic brains. Chinese Med J, 1996,109: 389-392.
  • 8Camilli PD, Miller P, Navone F, et al. Distribution of microtubule association protein 2 in the nervous system of the rat studied by immunofluorescence. Neurosci, 1984, 11: 819-846.
  • 9Emery JA, Roper SN, Rojiani AM. White matter neuronal heterotopia in temporal lobe epilepsy: A morphometric and immunohistochemical study. J Neuropathol Exp Neurol, 1997, 56: 1276-1282.
  • 10Yamanouchi H, Jay V, Otsubo H, et al. Early forms of microtubule-associated protein are strongly expressed in cortical dysplasia. Acta Neuropathol, 1998, 95: 466-470.

共引文献9

同被引文献21

  • 1Butmer B, Horstkorte R. Intracelluar ligands of NCAM. Adv Exp Med Biol, 2010, 663 (part 1) : 55-66.
  • 2Campod6nico PB, de Kier Joff6 ED, Urtreger AJ, et al. The neural cell adhesion molecule is involved in the metastatic ca- pacity in a murine model of lung cancer. Mol Carcinoq, 2010, 49(4) : 386-397.
  • 3Kilsdonk JW, Kempen LC, Muijen GN, et al. Soluble adhe- sion molecules in human cancers: sources and fates. Eur J Cell Biol, 2010, 89(6) : 415-427.
  • 4Ditlevsen DK, Povlsen GK, Berezin V, et al. NCAM-in- duced intracellular signaling revisited. J Neurosci Res, 2008, 86(4) : 727-743.
  • 5Conchonaud F, Nicolas S, Amoureux MC, et al. Polysialyla- tion increases lateral diffusion of neural cell adhesion molecule in the cell membrane. J Biol Chem, 2007, 282 (36): 26266 -26274.
  • 6Povlsen GK, Ditlevsen DK. The neural cell adhesion mole- cule NCAM and lipid rafts. Adv Exp Med Biol, 2010, 663 (part 3) : 183-198.
  • 7Ditlevsen DK, Kolkova K. Signaling pathways involved in NCAM-induced neurite outgrowth. Adv Exp Med Biol, 2010, 663: 151-168.
  • 8English AW. Cytokines, growth factors and sprouting at the neuromuscular junction. J Neurocytol, 2003 , 32 ( 5-8 ) : 943 -960.
  • 9Johnson CP, Fujimoto I, Rutishauser U, et al. Direct evi- dence that neural cell adhesion molecule (NCAM) polysialy- lation increases intermembrane repulsion and abrogates adhe- sion. J Biol Chem, 2005, 280(1) : 137-145.
  • 10Hansen SM, Berezin V, Bock E. Signaling mechanisms of neurite outgrowth induced by the cell adhesion molecules NCAM and N-cadherin. Cell Mol Life Sci, 2008, 65 (23) : 3809-3821.

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中风与神经疾病杂志
2008年 第3期

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