Hamon B, Audinat E, Gibelin N, Crépel F
Laboratoire de Neurobiologie et Neuropharmacologie du Développement, CNRS ERS F0100, Université Paris-sud, Orsay, France.
Exp Brain Res. 1995;107(2):197-204. doi: 10.1007/BF00230041.
Slowly inactivating outward currents were examined in neurons from rat anterior cortex dissociated at postnatal day 1 and recorded after 7-48 days in vitro by the use of whole-cell patch-clamp technique, in the presence of 0.5-0.8 microM tetrodotoxin (TTX). 50 microM carbachol and 1-5 mM CsCl2. Experiments were often carried out in the additional presence of 1-5 mM CsCl2, which blocks the anomalous, inwardly rectifying IQ, the fast Ca(2+)-dependent K+ current (IC), and 50 microM carbachol, which depresses the IM current. These currents were evoked by depolarizing steps to -40 +/- 5 mV from a conditioning hyperpolarization to -110 +/- 10 mV. Their sensitivity to elevation from 2.5 to 12.5 mM in extracellular K+ concentration, together with their sensitivity to 5-15 mM tetraethylammonium, suggests that they are mainly carried by K+ ions. Their activation and inactivation curves show that the threshold for activation is -65 mV, that their inactivation is achieved at -75 mV and that potentials more negative than -120 mV are needed to abolish it. The time-dependence of de-inactivation gives a maximal current amplitude for conditioning hyperpolarizations of 2 s and is best described by a monoexponential function with a time constant of 0.7 s. Slow transient K+ currents were depressed by low doses of 4-aminopyridine (30-100 microM), which indicates the occurrence of an ID-type component in the recorded K+ currents. No slowly declining K+ current was expressed when a recording solution containing 10 mM 1,2-bis (2-aminophenoxy)ethane-N,N,N'-N'-tetraacetic acid (BAPTA), instead of 1-5 mM BAPTA, was used. When recorded without Ca2+ chelator in the pipette, slowly declining K+ currents were blocked by bath-applied 40-50 microM BAPTA-aminoethoxy, revealing a large-amplitude, rapidly inactivating outward current. This residual component is insensitive to 50 microM 4-aminopyridine and may include a current more related to the IA-type. Our data provide evidence that, in cultured cortical neurons from rat, the expression of an ID-like K+ current is highly dependent on internal Ca2+ concentration.
利用全细胞膜片钳技术,在存在0.5 - 0.8微摩尔河豚毒素(TTX)、50微摩尔卡巴胆碱和1 - 5毫摩尔氯化铯(CsCl2)的条件下,对出生后第1天分离的大鼠前皮质神经元中缓慢失活的外向电流进行了研究。这些神经元在体外培养7 - 48天后进行记录。实验通常还在额外存在1 - 5毫摩尔氯化铯的情况下进行,氯化铯可阻断异常的内向整流IQ、快速的钙依赖性钾电流(IC);同时还存在50微摩尔卡巴胆碱,它可抑制IM电流。这些电流通过从 - 110 ± 10毫伏的预超极化去极化至 - 40 ± 5毫伏的步骤来诱发。它们对细胞外钾离子浓度从2.5毫摩尔升高到12.5毫摩尔的敏感性,以及对5 - 15毫摩尔四乙铵的敏感性表明,它们主要由钾离子携带。它们的激活和失活曲线表明,激活阈值为 - 65毫伏,失活在 - 75毫伏时达到,并且需要比 - 120毫伏更负的电位才能消除失活。去失活的时间依赖性在2秒的预超极化时给出最大电流幅度,并且最好用时间常数为0.7秒的单指数函数来描述。低剂量的4 - 氨基吡啶(30 - 100微摩尔)可抑制缓慢的瞬时钾电流,这表明在记录的钾电流中存在ID型成分。当使用含有10毫摩尔1,2 - 双(2 - 氨基苯氧基)乙烷 - N,N,N' - N' - 四乙酸(BAPTA)而非1 - 5毫摩尔BAPTA的记录溶液时,未表达缓慢下降的钾电流。当移液管中没有钙螯合剂进行记录时,浴加40 - 50微摩尔BAPTA - 氨基乙氧基可阻断缓慢下降的钾电流,揭示出一个大振幅、快速失活的外向电流。这个残余成分对50微摩尔4 - 氨基吡啶不敏感,可能包括一个与IA型更相关的电流。我们的数据提供了证据,表明在大鼠培养的皮质神经元中,ID样钾电流的表达高度依赖于细胞内钙浓度。