镧对大鼠海马神经元瞬时外向和延迟整流钾通道的调控作用(英文)  

Modulation of transient outward and delayed rectifier potassium channels in acutely isolated hippocampal neurons by La^(3+)

作　　者：王增贤[1] 陈明[1] 孙伟[1] 杨频[2] 

机构地区：[1]泰山医学院神经生物学教研室,山东泰安271000 [2]山西大学分子科学研究所化学生物学与分子工程教育部重点实验室,山西太原030006

出　　处：《泰山医学院学报》2012年第8期561-568,共8页Journal of Taishan Medical College

基　　金：National Natural Science Foundation of China(No.20637010)

摘　　要：目的研究细胞内外La3+对急性分离大鼠海马神经元IA、IK电流的影响。方法运用全细胞膜片钳技术记录细胞内外施加La3+后IA、IK的变化。结果细胞外100μmol/L La3+使IA稳态激活曲线和稳态失活曲线半数电压向去极化方向移动,IA失活恢复时间延长,IA激活动力学抑制。细胞内100μmol/L La3+使IK稳态激活曲线左移,并减弱了细胞外La3+引起的IA稳态失活曲线右移程度。结论细胞内外La3+可能与IA、IK通道蛋白某些位点结合而发挥对通道蛋白的调控作用,细胞外La3+对IA通道蛋白的多个状态都有影响,并且细胞外La3+对IA稳态失活的部分作用可能通过第二信使实现。Objective： To study the modulation of transient outward and delayed rectifier potassium channels in acutely i- solatod hippocampal neurons by La^3＋. Methods：The effects of extraeellular and intracellular La^3＋ on the IA, IK of hipp- ocampal neurons were investigated using the whole-cell patch-clamp technique. Resuhs：Extracellular 100 μM La3 ~ inhibi- ted Is but failed to affect Ix. The vohage midpoint of steady-state activation and inactivation curves of Is was shifted to a de- polarized state and the activation of kinetics was suppressed by extracellular La^3＋. Extracellular La^3＋ slowed the kinetics of recovery of IA from inactivation. Intracellular 100 ~M La^3＋ caused a hyperpolarizing shift in the voltage midpoint of the steady-state activation of Ix. Intracellular 100 μM La^3＋. affected the modulation of steady-state inactivation by extracellular 100 μM La^3＋. Conclusion：The results indicated that the IA and Ik values of hippocampal neurons might be modulated by extraceLlular and intracellular La^3＋ binding to particular sites of potassium channel proteins. Thus, extracellular La^3＋ could influence the steady-state inactivation of IA in part through an intracellular second messenger.

关 键 词：镧 钾通道 全细胞膜片钳技术 海马神经元 

分 类 号：R363[医药卫生—病理学]