DeCoursey T E, Cherny V V
Department of Molecular Biophysics and Physiology, Rush Presbyterian St. Luke's Medical Center, Chicago, Illinois 60612, USA.
J Gen Physiol. 1998 Oct;112(4):503-22. doi: 10.1085/jgp.112.4.503.
H+ currents in human neutrophils, rat alveolar epithelial cells, and several mammalian phagocyte cell lines were studied using whole-cell and excised-patch tight-seal voltage clamp techniques at temperatures between 6 and 42 degrees C. Effects of temperature on gating kinetics were distinguished from effects on the H+ current amplitude. The activation and deactivation of H+ currents were both highly temperature sensitive, with a Q10 of 6-9 (activation energy, Ea, approximately 30-38 kcal/mol), greater than for most other ion channels. The similarity of Ea for channel opening and closing suggests that the same step may be rate determining. In addition, when the turn-on of H+ currents with depolarization was fitted by a delay and single exponential, both the delay and the time constant (tauact) had similarly high Q10. These results could be explained if H+ channels were composed of several subunits, each of which undergoes a single rate-determining gating transition. H+ current gating in all mammalian cells studied had similarly strong temperature dependences. The H+ conductance increased markedly with temperature, with Q10 >/= 2 in whole-cell experiments. In excised patches where depletion would affect the measurement less, the Q10 was 2.8 at >20 degrees C and 5.3 at <20 degrees C. This temperature sensitivity is much greater than for most other ion channels and for H+ conduction in aqueous solution, but is in the range reported for H+ transport mechanisms other than channels; e.g., carriers and pumps. Evidently, under the conditions employed, the rate-determining step in H+ permeation occurs not in the diffusional approach but during permeation through the channel itself. The large Ea of permeation intrinsically limits the conductance of this channel, and appears inconsistent with the channel being a water-filled pore. At physiological temperature, H+ channels provide mammalian cells with an enormous capacity for proton extrusion.
利用全细胞膜片钳和切除膜片紧密封接电压钳技术,在6至42摄氏度的温度范围内,对人中性粒细胞、大鼠肺泡上皮细胞和几种哺乳动物吞噬细胞系中的H⁺电流进行了研究。温度对门控动力学的影响与对H⁺电流幅度的影响得以区分。H⁺电流的激活和失活均对温度高度敏感,Q10为6 - 9(活化能,Ea,约30 - 38千卡/摩尔),高于大多数其他离子通道。通道开放和关闭的Ea相似,表明相同步骤可能是速率决定步骤。此外,当用延迟和单指数拟合去极化时H⁺电流的开启过程时,延迟和时间常数(tauact)具有相似的高Q10。如果H⁺通道由几个亚基组成,每个亚基经历单个速率决定门控转变,这些结果就能得到解释。在所研究的所有哺乳动物细胞中,H⁺电流门控具有相似的强温度依赖性。在全细胞实验中,H⁺电导随温度显著增加,Q10≥2。在切除膜片中,耗尽对测量影响较小,在>20摄氏度时Q10为2.8,在<20摄氏度时为5.3。这种温度敏感性远高于大多数其他离子通道以及水溶液中H⁺传导的情况,但处于报道的除通道外其他H⁺转运机制(如载体和泵)的范围内。显然,在所采用的条件下,H⁺渗透的速率决定步骤不是发生在扩散过程中,而是在通过通道本身的渗透过程中。渗透的大Ea本质上限制了该通道的电导,并且似乎与通道是充满水的孔不一致。在生理温度下,H⁺通道为哺乳动物细胞提供了巨大的质子外排能力。