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目的 研究 L i+ 对非洲爪蟾卵母细胞表达的双基因内向整流钾通道 (IRK1- T)的作用及其机制 .方法 采用双微电极电压钳 (TEV)法 .结果 细胞外 K+浓度为 10 mmol·L- 1时 ,细胞外 L i+可加速 IRK1- T内向电流的失活过程 ;3个指数拟合的分析结果表明 :由于细胞外 L i+对失活过程的时间常数几乎无影响 ,因此 L i+ 对失活过程的作用是通过 L i+ 与K+在 IRK1- T上相互竞争同一结合位点而造成的 .细胞外L i+ 对 IRK1- T的瞬间内向电流 (施加电压后 1ms)具有时间依赖性和电压依赖性的易化作用 ,增加细胞外 K+ 浓度与 L i+浓度的比率 ,这一易化作用增强 ,表明 L i+加速 IRK1- T内向电流的失活过程的作用因 L i+浓度相对下降而减少 .细胞外L i+ 对外向电流几乎无作用 ;L i+ 对 IRK1- T的门控特性几乎无影响 ;因为在细胞外加入 L i+后反转电位几乎不变 ,所以IRK1- T对 L i+不通透 .结论 L i+不仅是一快速通道阻断剂 ,而且细胞外 L i+ 还可以在增大 IRK1- T的内向整流作用的同时缩短该电流的时程
Objective To investigate the effect and mechanism of L i + on bifunctional inward rectifier potassium channel (IRK1-T) expressed in Xenopus laevis oocytes.Methods Double-electrode voltage clamp (TEV) method was used.Results The extracellular K + concentration was 10 mmol · L-1 extracellular L i + can accelerate the inactivation of IRK1-T inward current. The analysis of the three exponential fitting results shows that since the extracellular L i + has almost no effect on the inactivation time constant, L The effect of i + on the inactivation process is due to the fact that L i + and K + compete with each other for the same binding site on IRK1-T. The extracellular L i + has a time-dependent inward current to IRK1-T (1 ms after voltage application) And voltage-dependent facilitation, increasing the ratio of extracellular K + concentration to L i + concentration, this facilitation being enhanced, suggesting that the effect of L i + on the inactivation of IRK1-T inward current due to a relative decrease in L i + concentration L i + has little effect on the outward current; L i + has almost no effect on the gating properties of IRK1-T; since the reversal potential is almost constant after addition of L i + extracellularly, IRK1-T vs. L i + Transparent. Conclusion L i + is not only A fast channel blocker, and extracellular Li + can also shorten the current time course while increasing the inward rectification of IRK1-T