期刊文献+

Sombati癫癎细胞模型电压依赖性钾电流的变化

Changes of Voltage-dependent Potassium Current in Sombati Cell Model of Epilepsy
原文传递
导出
摘要 目的:采用全细胞膜片钳记录技术研究Sombati癫癎细胞模型电压依赖性K+电流的变化。方法:取SD新生乳鼠双侧海马,体外原代培养海马神经元,培养至第9天的部分海马神经元经无镁液处理3h制备癫癎细胞模型,采用全细胞膜片钳技术分别记录正常组(未经无镁液处理的海马神经元)和致癎组(经无镁液处理3h后更换为正常维持培养液的海马神经元)海马神经元的电压依赖性外向K+电流。结果:致癎组外向K+电流比正常组增大,峰值电流由(596.62±79.23)pA增至(978.68±53.23)pA,两组间比较差异有统计学意义(P=0.000)。与正常组相比,致癎组的I-V曲线明显左移,I-V曲线形态无显著改变。结论:Sombati癫癎细胞模型中,电压依赖性外向K+电流显著增加可能是癫癎细胞模型癎性放电后为了保持细胞稳态的代偿性保护作用。 Aim:To study the changes of voltage-dependent K+ current in Sombati cell model of epilepsy by using whole-cell patch clamp technique.Methods:The hippocampal tissues were sampled from 1-day-old SD rats and used for the primary culture of hippocampus neurons in vitro.After 9 days of primary culture,the hippocampal neurons were randomly divided into two groups:the normal group and the epilepsy group,which voltage-dependent K+ current were recorded by whole cell patch clamp technique respectively.Results:The K+ currents in the epilepsy group increased significantly than that in the normal group,and the peak current in the epilepsy group increased from(596.62±79.23) pA to(596.62±79.23) pA(P=0.000).The differences were significant statistically between the two groups.Compared with the normal group,I-V curve of the epilepsy group was shifted to the left obviously,but the shape of the curve remained unchanged.Conclusion:The voltage-dependent outward K+ current in Sombati cell model of epilepsy increased significantly,which may be the result of maintaining compensatory protective effect on cell homeostasis after discharge.
出处 《中国临床神经科学》 2011年第5期449-453,共5页 Chinese Journal of Clinical Neurosciences
基金 国家自然科学基金课题(编号:30960111) 广西科技厅面上项目(编号:2010GXNSFA013168)
关键词 电压依赖性K+电流 癫癎细胞模型 全细胞膜片钳技术 海马神经元 voltage-dependent K+ current cell model of epilepsy patch-clamp technique
  • 相关文献

参考文献20

  • 1Sombati S,Delorenzo RJ,Recurrent spontaneous seizure activity in hippocampal neuronal networks in culture[J].J Neurophysiol,1995,73:1706-1711.
  • 2马美刚,吴原,苏婕,吴月娟,刘秀颖,唐玉兰,余璐.难治性癫痫细胞模型中Lamininβ1的表达及意义[J].中风与神经疾病杂志,2010,27(10):886-889. 被引量:2
  • 3Nunez J.Primary Culture of Hippocampal Neurons from PO New-born Rats[J].J Vis Exp,2008,pii:895.doi:10.3791/895.
  • 4Wang Y,Shi X,Qi Z.Hypericin prolongs action potential duration in hippocampal neurons by acting on K+ channels[J].Br J Pharmacol,2010,159:1402-1407.
  • 5Netzer P,Domek M,Pai R,et al.Inhibition of human colon cancer cell growth by antisense oligodeoxynucleotides targeted at basic fibroblast growth factor[J].Aliment Pharmacol Ther,2001,15:1673-1679.
  • 6Mohapatra DP,Misonou H,Pan SJ,et al.Regulation of intrinsic excitability in hippocampal neurons by activity-dependent modu-lation of the KV2.1 potassium channel[J].Channels (Austin),2009,3:46-56.
  • 7Delorenzo RJ,Sombati S,Coulter DA.Effects of topiramate on sustained repetitive firing and spontaneous recurrent seizure dis-charges in cultured hippocampal neurons[J].Epilepsia,2000,Suppl 1:S40-S44.
  • 8赵秀鹤,迟兆富,尚伟,迟令懿.无镁诱导体外培养人胚海马神经元癫痫样放电的实验[J].中国病理生理杂志,2007,23(5):1031-1033. 被引量:8
  • 9Deshpande LS,Nagarkatti N,Sombati S,et al.The novel antiepileptic drug carisbamate (RWJ 333369) is effective in inhibiting spontaneous recurrent seizure discharges and blocking sustained repetitive firing in cultured hippocampal neurons[J].Epilepsy Res,2008,79:158-165.
  • 10常好会,苏涛,孙卫文,赵绮华,秦兵,廖卫平.钾离子通道Kv4.2、Kv4.3及其相互作用蛋白KChIP1在电点燃癫模型中的表达变化[J].中华医学杂志,2006,86(47):3315-3318. 被引量:5

二级参考文献67

  • 1赵秀鹤,迟兆富,尚伟,迟令懿.无镁诱导体外培养人胚海马神经元癫痫样放电的实验[J].中国病理生理杂志,2007,23(5):1031-1033. 被引量:8
  • 2吴逊.癫痫和发作性疾病.第13卷.北京:人民军医出版社,2001,27-32.
  • 3Bassi MT, Balottin U, Panzeri C, et al. Functional analysis of novel KCNQ2 and KCNQ3 gene variants found in a large pedigree With benign familial neonatal convulsions ( BFNC ). Neurogenetics, 2005, 6(4) : 185-193.
  • 4Yalcin O, Caglayan SH, Sahik S, et al. A novel missense mutation (N258S) in the KCNQ2 gene in a Turkish family afflicted with benign familial neonatal convulsions ( BFNC ). Turk J Pediatr, 2007, 49(4) : 385-389.
  • 5Soldovieri MV, Cilio MR, Miceli F, et al. Atypical gating of M-type potassium channels conferred by mutations in uncharged residues in the S4 region of KCNQ2 causing benign familial neonatal convulsions. Neurosci, 2007 , 27 ( 18 ) :4919-4928.
  • 6Neubauer BA, Waldegger S, Heinzinger J, et al. KCNQ2 and KCNQ3 mutations contribute to different idiopathic epilepsy syndromes. Neurology, 2008, 71(3) : 177-183.
  • 7Hou PA, Huang P, Hansen CB, et al. Impermeability of the GIRK2 weaver channel to divalent cations. Am J Physiol Cell Physiol, 2000, 278(5): 1038-1046.
  • 8Dai AI, Wasay M. Idiopathic epilepsy of childhood and potassium ion channels. Pak Med Assoc, 2007, 57 (8): 415-418.
  • 9Thaur ML, Sheug M, Lowenstein DH, et al. Differential expression of K + channel mRNAs in the rat brain and dowm- regulation in the hippocampus following seizures. Neuron, 1992, 8(6): 1055-1067
  • 10Meech RW. Calcium-mediated potassium activation in Helix neurones. Physiol, 1974 , 237 (2) : 43-44.

共引文献26

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部