CAJ | 학술논문

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100 μmol/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100 μmol/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.
목적 연구세포내외La3+대급성분리대서해마신경원IA、IK전류적영향.방법 운용전세포막편겸기술기록세포내외시가La3+후IA、IK적변화.결과 세포외100 μmol/L La3+사IA은태격활곡선화은태실활곡선반수전압향거겁화방향이동, IA실활회복시간연장, IA격활동역학억제.세포내100 μmol/L La3+사IK은태격활곡선좌이,병감약료세포외La3+인기적IA은태실활곡선우이정도.결론 세포내외La3+가능여IA、IK통도단백모사위점결합이발휘대통도단백적조공작용,세포외La3+대 IA통도단백적다개상태도유영향,병차세포외La3+대IA은태실활적부분작용가능통과제이신사실현.
Objective:To study the modulation of transient outward and delayed rectifier potassium channels in acutely isolated hippocampal neurons by La3+.Methods:The effects of extracellular and intracellular La3+ on the IA, IK of hippocampal neurons were investigated using the whole-cell patch-clamp technique. Results:Extracellular 100 μM La3+ inhibited IA but failed to affect IK. The voltage midpoint of steady-state activation and inactivation curves of IA was shifted to a depolarized state and the activation of kinetics was suppressed by extracellular La3+. Extracellular La3+ slowed the kinetics of recovery of IA from inactivation. Intracellular 100 μM La3+ caused a hyperpolarizing shift in the voltage midpoint of the steady-state activation of IK. Intracellular 100 μM La3+ affected the modulation of steady-state inactivation by extracellular 100 μM La3+. Conclusion:The results indicated that the IA and IK values of hippocampal neurons might be modulated by extracellular and intracellular La3+ binding to particular sites of potassium channel proteins. Thus, extracellular La3+ could influence the steady-state inactivation of IA in part through an intracellular second messenger.