The Nora Eccles Harrison Cardiovascular Research & Training Institute, University of Utah, 95 South 2000 East, Salt Lake City, UT 84112, USA.
Pflugers Arch. 2011 Jan;461(1):91-7. doi: 10.1007/s00424-010-0894-1. Epub 2010 Oct 28.
Previous studies have shown that lidocaine and other local anesthetic drugs (LAs) cause use-dependent block of sodium current (I (Na)), i.e., block that increases with membrane depolarization by allosteric coupling between drug binding in the inner pore and the S4s in domains III and IV. MTSET protection experiments have established that LAs stabilize DIIIS4 in an outward, depolarized position. Similar tests have not been reported for the DIVS4, although LAs have been shown to reduce DIV's contribution to total gating charge by about one third and to alter its movement such that it contributes more gating charge at negative potentials around -100 mV compared to non-drug-bound sodium (Na) channels. To investigate whether lidocaine reduces the gating charge of DIVS4 by causing it to adopt either a depolarized position at rest or by restricting its outward movement upon depolarization, we performed MTSET protection experiments on I (Na) of the mutant Na channel, R1628C (R3C-DIV), in the presence and absence of 10 mM lidocaine. The results indicate that lidocaine causes the DIVS4 to assume a more depolarized position, which facilitates its movement upon depolarization leading to the excess gating charge at potentials near -100 mV.
先前的研究表明,利多卡因和其他局部麻醉药物(LA)会导致钠电流(I(Na))的使用依赖性阻滞,即通过药物结合在内孔中的变构偶联以及 III 和 IV 域中的 S4 之间的变构偶联,随着膜去极化而增加的阻滞。MTSET 保护实验已经证实,LA 将 DIIIS4 稳定在向外的去极化位置。尽管已经表明 LA 会降低 DIV 对总门控电荷的贡献约三分之一,并改变其运动,使其在相对于非药物结合的钠(Na)通道的约-100 mV 的负电位下贡献更多的门控电荷,但尚未有关于 DIVS4 的类似测试报告。为了研究利多卡因是否通过使 DIVS4 在静止时采用去极化位置或通过限制其在去极化时的外向运动来减少 DIVS4 的门控电荷,我们在存在和不存在 10 mM 利多卡因的情况下,对突变 Na 通道 R1628C(R3C-DIV)的 I(Na)进行了 MTSET 保护实验。结果表明,利多卡因使 DIVS4 处于更去极化的位置,这促进了其在去极化时的运动,导致在接近-100 mV 的电位下出现过多的门控电荷。