Wang Yi-Chi, Huang Rong-Chi
Department of Physiology and Pharmacology, Chang Gung University School of Medicine, Tao-Yuan, Taiwan.
J Neurophysiol. 2006 Jul;96(1):109-18. doi: 10.1152/jn.01369.2005. Epub 2006 Feb 8.
Cell-attached and whole cell recording techniques were used to study the effects of electrogenic sodium pump on the excitability of rat suprachiasmatic nucleus (SCN) neurons. Blocking the sodium pump with the cardiac steroid strophanthidin or zero K+ increased the spontaneous firing of SCN neurons to different degrees with different recording modes, whereas turning the sodium pump into a nonselective cation channel with the marine toxin palytoxin invariably increased the spontaneous firing to the point of total blockade. Current-clamp recordings indicated that strophanthidin increased the rate of membrane depolarization and reduced the peak afterhyperpolarization potential (AHP), whereas zero K+ also increased the rate of depolarization, but enhanced the peak AHP. The dual effect of zero K+ was reflected by the biphasic time course of voltage responses to zero K+: an inhibitory phase with enhanced peak AHP and slower firing, followed by a delayed excitatory phase with faster rate of membrane depolarization and faster firing. In the presence of strophanthidin to block the sodium pump, zero K+ consistently decreased firing by enhancing the peak AHP. Repetitive applications of K+ -free solution gradually turned the biphasic inhibitory-followed-by-excitatory voltage response into a monophasic inhibitory response in cells recorded with the whole cell (but not the cell-attached) mode, suggesting rundown of sodium pump activity. Taken together, the results suggest that spontaneous firing of SCN neurons is regulated by sodium pump activity as well as the AHP, and that sodium pump activity is modulated by intracellular soluble substances subject to rundown under the whole cell conditions.
采用细胞贴附式和全细胞记录技术，研究电生钠泵对大鼠视交叉上核（SCN）神经元兴奋性的影响。用强心甾类药物毒毛花苷阻断钠泵或采用零钾溶液，在不同记录模式下，SCN神经元的自发放电均有不同程度增加；而用海葵毒素岩沙海葵毒素将钠泵转变为非选择性阳离子通道时，自发放电总是增加至完全阻滞的程度。电流钳记录显示，毒毛花苷增加膜去极化速率并降低超极化后电位（AHP）峰值，而零钾溶液也增加去极化速率，但增强AHP峰值。零钾溶液的双重作用体现在对零钾溶液电压反应的双相时间进程中：先是抑制相，AHP峰值增强且放电减慢，随后是延迟的兴奋相，膜去极化速率加快且放电加快。在存在毒毛花苷阻断钠泵的情况下，零钾溶液通过增强AHP峰值持续降低放电频率。在全细胞（而非细胞贴附式）记录模式下，重复应用无钾溶液会使双相抑制后兴奋的电压反应逐渐转变为单相抑制反应，提示钠泵活性降低。综上所述，结果表明SCN神经元的自发放电受钠泵活性以及AHP的调节，且钠泵活性受细胞内可溶性物质的调节，在全细胞条件下会降低。
