Engberg I, Flatman J A, Lambert J D
Br J Pharmacol. 1984 Jan;81(1):215-24. doi: 10.1111/j.1476-5381.1984.tb10763.x.
QX-222 (the trimethyl analogue of lignocaine), methylxylocholine, lignocaine and pentobarbitone were iontophoresed intracellularly into cat lumbosacral motoneurones. Iontophoresis and recording was either from a triple-barrelled microelectrode unit or from two separately advanced microelectrodes. QX-222 and methylxylocholine caused a very slow reversible block of the current-evoked and antidromic action potentials (AP) with no significant change of membrane potential (EM). Lignocaine had a minimal blocking effect on the AP. No change, or only a small decrease, of membrane slope conductance (GM) was seen when the APs had been totally abolished. QX-222 and methylxylocholine reduced the massive GM increase evoked by the passage of large depolarizing currents and converted the post-current hyperpolarization (time constant 120-150 ms) into a depolarization of similar time course. It is suggested that the quaternary local anaesthetics can reduce the fast and slow voltage-dependent potassium conductances. Both agents totally blocked AP generation without decreasing the magnitude of the Ia e.p.s.p. It is suggested that intracellularly iontophoresed QX-222 (on account of its low lipid solubility) could be used as a pharmacological tool to block specifically the active Na and channels in only the cell impaled by the microelectrodes.
QX - 222(利多卡因的三甲基类似物)、甲基东莨菪碱、利多卡因和戊巴比妥通过离子电渗法细胞内注入猫腰骶部运动神经元。离子电渗法和记录要么通过三管微电极装置进行,要么通过两个单独推进的微电极进行。QX - 222和甲基东莨菪碱引起电流诱发动作电位和逆向动作电位(AP)非常缓慢的可逆性阻断,而膜电位(EM)无明显变化。利多卡因对动作电位的阻断作用最小。当动作电位完全消失时,膜斜率电导(GM)未见变化或仅略有下降。QX - 222和甲基东莨菪碱减少了由大的去极化电流通过所诱发的GM大量增加,并将电流后超极化(时间常数120 - 150毫秒)转变为类似时间进程的去极化。提示季铵类局部麻醉药可降低快速和慢速电压依赖性钾电导。两种药物都完全阻断了动作电位的产生,而不降低Ia兴奋性突触后电位(e.p.s.p.)的幅度。提示细胞内离子电渗法注入的QX - 222(由于其低脂溶性)可作为一种药理学工具,仅特异性阻断被微电极刺入的细胞中的活性钠通道。