Cherny V V, Markin V S, DeCoursey T E
Department of Molecular Biophysics and Physiology, Rush Presbyterian St. Luke's Medical Center, Chicago, Illinois 60612, USA.
J Gen Physiol. 1995 Jun;105(6):861-96. doi: 10.1085/jgp.105.6.861.
Voltage-activated H+ currents were studied in rat alveolar epithelial cells using tight-seal whole-cell voltage clamp recording and highly buffered, EGTA-containing solutions. Under these conditions, the tail current reversal potential, Vrev, was close to the Nernst potential, EH, varying 52 mV/U pH over four delta pH units (delta pH = pHo - pHi). This result indicates that H+ channels are extremely selective, PH/PTMA > 10(7), and that both internal and external pH, pHi, and pHo, were well controlled. The H+ current amplitude was practically constant at any fixed delta pH, in spite of up to 100-fold symmetrical changes in H+ concentration. Thus, the rate-limiting step in H+ permeation is pH independent, must be localized to the channel (entry, permeation, or exit), and is not bulk diffusion limitation. The instantaneous current-voltage relationship exhibited distinct outward rectification at symmetrical pH, suggesting asymmetry in the permeation pathway. Sigmoid activation kinetics and biexponential decay of tail currents near threshold potentials indicate that H+ channels pass through at least two closed states before opening. The steady state H+ conductance, gH, as well as activation and deactivation kinetic parameters were all shifted along the voltage axis by approximately 40 mV/U pH by changes in pHi or pHo, with the exception of the fast component of tail currents which was shifted less if at all. The threshold potential at which H+ currents were detectably activated can be described empirically as approximately 20-40(pHo-pHi) mV. If internal and external protons regulate the voltage dependence of gH gating at separate sites, then they must be equally effective. A simpler interpretation is that gating is controlled by the pH gradient, delta pH. We propose a simple general model to account for the observed delta pH dependence. Protonation at an externally accessible site stabilizes the closed channel conformation. Deprotonation of this site permits a conformational change resulting in the appearance of a protonation site, possibly the same one, which is accessible via the internal solution. Protonation of the internal site stabilizes the open conformation of the channel. In summary, within the physiological range of pH, the voltage dependence of H+ channel gating depends on delta pH and not on the absolute pH.
利用紧密封接全细胞电压钳记录技术和含有高缓冲剂、乙二醇双乙醚二胺四乙酸(EGTA)的溶液,对大鼠肺泡上皮细胞中的电压激活H⁺电流进行了研究。在这些条件下,尾电流反转电位Vrev接近能斯特电位EH,在四个pH单位变化范围内(ΔpH = pHo - pHi),每单位pH变化52 mV。该结果表明H⁺通道具有极高的选择性,PH/PTMA > 10⁷,并且细胞内和细胞外pH,即pHi和pHo,均得到良好控制。尽管H⁺浓度有高达100倍的对称变化,但在任何固定的ΔpH下,H⁺电流幅度实际上是恒定的。因此,H⁺通透的限速步骤与pH无关,一定位于通道处(进入、通透或流出),而不是由大量扩散限制所致。在对称pH条件下,瞬时电流-电压关系呈现出明显的外向整流,表明通透途径存在不对称性。S形激活动力学和接近阈值电位时尾电流的双指数衰减表明,H⁺通道在开放前至少经过两个关闭状态。通过改变pHi或pHo,稳态H⁺电导gH以及激活和失活动力学参数均沿电压轴大约移动40 mV/单位pH,但尾电流的快速成分移动较少或根本不移动。可检测到H⁺电流被激活的阈值电位经验性地描述为大约20 - 40(pHo - pHi)mV。如果细胞内和细胞外质子在不同位点调节gH门控的电压依赖性,那么它们的作用必定相同。一种更简单的解释是,门控由pH梯度ΔpH控制。我们提出一个简单的通用模型来解释观察到的对ΔpH的依赖性。在外部可及位点的质子化稳定了通道关闭构象。该位点的去质子化允许构象改变,导致出现一个质子化位点,可能是同一个位点,它可通过细胞内溶液到达。细胞内位点的质子化稳定了通道的开放构象。总之,在生理pH范围内,H⁺通道门控的电压依赖性取决于ΔpH,而不是绝对pH。