Mathias R T, Cohen I S, Oliva C
Department of Physiology and Biophysics, State University of New York, Stony Brook 11794.
Biophys J. 1990 Sep;58(3):759-70. doi: 10.1016/S0006-3495(90)82418-8.
Recent experimental studies (Pusch and Neher, 1988) and theoretical studies (Oliva et al., 1988) have found that the pipette tip is a significant barrier to diffusion in the whole cell patch clamp configuration. In this paper, we extend the theoretical analysis of fluxes between the pipette and cell to include transmembrane fluxes. The general conclusions are: (a) within the pipette, ion fluxes are driven primarily by diffusion rather than voltage gradients. (b) At steady state there is a concentration difference between the bulk pipette and intracellular solution that is described by delta c = jRp/Dp, where delta c = 1 mM for a flux, j = 1 fmol/s, through a pipette of resistance, Rp = 1 M omega, filled with a solution of resistivity, p = 100 omega --cm, given a solute diffusion coefficient, D = 10(-5) cm2/s. (c) The time to steady state is always accelerated by membrane transport, regardless of the direction of transport. We apply our analysis to the measurement of transport by the Na/K pump and Na/Ca exchanger in cells from the ventricles of mammalian heart. We find that the binding curve for intracellular Na+ to the Na/K pump will appear significantly less steep and more linear if one does not correct for the concentration difference between intracellular and pipette Na+. Similar shifts in the binding curve for extracellular Na+ to the Na/Ca exchanger can occur due to depletion of intracellular Ca(+)+ when the exchanger is stimulated. Lastly, in Appendix we analyze the effects of mobile and fixed intracellular buffers on the movement of Ca(+)+ between the pipette and cell. Fixed buffers greatly slow the time for equilibration of pipette and intracellular Ca(+)+. Mobile buffers act like a shuttle system, as they carry Ca(+)+ from pipette to cell then diffuse back when they are empty. Vigorous transport by the Na/Ca exchanger depletes mobile buffered calcium, thus stimulating diffusion from the pipette to match the rate of Ca(+)+ transport. Moreover, we find that binding of Ca(+)+ to the exchanger can be affected by the mobile buffer.
最近的实验研究(普施和内尔,1988年)和理论研究(奥利瓦等人,1988年)发现,在全细胞膜片钳配置中,移液器尖端是扩散的一个重要障碍。在本文中,我们扩展了对移液器和细胞之间通量的理论分析,以包括跨膜通量。总体结论如下:(a) 在移液器内,离子通量主要由扩散驱动,而非电压梯度。(b) 在稳态时,移液器主体与细胞内溶液之间存在浓度差,其由δc = jRp/Dp描述,其中对于通过电阻Rp = 1 MΩ、填充有电阻率p = 100 Ω·cm的溶液、溶质扩散系数D = 10(-5) cm2/s的移液器的通量j = 1 fmol/s,δc = 1 mM。(c) 无论运输方向如何膜运输总是会加速达到稳态的时间。我们将我们的分析应用于哺乳动物心脏心室细胞中钠钾泵和钠钙交换器的运输测量。我们发现,如果不校正细胞内和移液器内钠离子之间的浓度差,细胞内钠离子与钠钾泵的结合曲线将显得明显不那么陡峭且更呈线性。当刺激交换器时,由于细胞内钙离子耗尽,细胞外钠离子与钠钙交换器的结合曲线可能会出现类似的偏移。最后,在附录中,我们分析了可移动和固定的细胞内缓冲剂对移液器和细胞之间钙离子移动的影响。固定缓冲剂大大减慢了移液器和细胞内钙离子平衡的时间。可移动缓冲剂的作用类似于穿梭系统,因为它们将钙离子从移液器携带到细胞,然后在排空时扩散回来。钠钙交换器的剧烈运输会耗尽可移动缓冲的钙,从而刺激从移液器扩散以匹配钙离子运输速率。此外,我们发现钙离子与交换器的结合会受到可移动缓冲剂的影响。