Brown H F, Kimura J, Noble D, Noble S J, Taupignon A
Proc R Soc Lond B Biol Sci. 1984 Sep 22;222(1228):329-47. doi: 10.1098/rspb.1984.0067.
The membrane currents underlying the pacemaker depolarization have been investigated in rabbit s.a. node preparations using the two-microelectrode voltage clamp technique. Many of the experimental results have been simulated using a computer model of s.a. node electrical activity. Changes of three time-dependent membrane currents which could contribute to pacemaker depolarization are found to occur in the relevant potential range: decay of the potassium current, iK, and activation of the inward current, if, and of the slow inward current, isi. The contribution of if activation to the pacemaker depolarization ranges from nil to an appreciable part depending on the preparation; when Cs (1 mM) blocks if, it nevertheless does not prevent pacemaking. In the model, holding the if activation variable at zero slows but does not stop pacemaking; doubling if conductance and shifting its activation curve by 15 mV in the positive direction causes a 15% faster rate of pacemaking. The slow time course of re-availability of isi must be allowed for when determining the isi threshold. A voltage clamp protocol designed to mimic as closely as possible an action potential followed by a pacemaker depolarization gives an estimate of isi threshold at the potential level of the last third of the pacemaker depolarization. This has been confirmed in experiments in which the voltage clamp was switched on at different points in the pacemaker depolarization. In the computer simulation, 'blocking' isi depolarizes the membrane to the zero current level (close to the potential reached at the end of a pacemaker depolarization) and stops the generation of action potentials. The decay of iK contributes to the pacemaker depolarization; with both our own model and that of K. Yanagihara, A. Noma and H. Irisawa, Jap. J. Physiol. 30, 841-857 (1980) 'blocking' iK decay abolishes pacemaker activity. Computations of extracellular K+ concentration changes compared with iK decay in a cylindrical model allow re-assessment of the interpretation of K+ concentration measurements during pacemaking made by J. Maylie, M. Morad and J. Weiss, J. Physiol., Lond. 311, 167-178 (1981).(ABSTRACT TRUNCATED AT 400 WORDS)
利用双微电极电压钳技术,在兔窦房结标本中研究了起搏去极化所涉及的膜电流。许多实验结果已通过窦房结电活动的计算机模型进行模拟。发现在相关电位范围内,三种与时间相关的膜电流发生变化,这些变化可能导致起搏去极化:钾电流(iK)的衰减、内向电流(if)和缓慢内向电流(isi)的激活。if激活对起搏去极化的贡献因标本而异,范围从无到相当一部分;当1 mM的铯阻断if时,仍不能阻止起搏。在模型中,将if激活变量设为零会减慢但不会停止起搏;将if电导加倍并使其激活曲线正向移动15 mV会使起搏速率加快15%。在确定isi阈值时,必须考虑isi再激活的缓慢时间进程。一个旨在尽可能模拟动作电位后跟随起搏去极化的电压钳方案,给出了在起搏去极化最后三分之一电位水平时的isi阈值估计。这已在实验中得到证实,即在起搏去极化的不同点开启电压钳。在计算机模拟中,“阻断”isi会使膜去极化到零电流水平(接近起搏去极化结束时达到的电位)并停止动作电位的产生。iK的衰减有助于起搏去极化;在我们自己的模型以及柳原K、野间A和入泽H(《日本生理学杂志》30,841 - 857,1980)的模型中,“阻断”iK衰减都会消除起搏活动。在圆柱形模型中,将细胞外钾离子浓度变化与iK衰减进行比较的计算,使得对梅利J、莫拉德M和韦斯J(《伦敦生理学杂志》311,167 - 178,1981)在起搏过程中钾离子浓度测量结果的解释得以重新评估。(摘要截取自400字)