Laurent G
Department of Zoology, University of Cambridge, England.
J Neurosci. 1991 Jun;11(6):1713-26. doi: 10.1523/JNEUROSCI.11-06-01713.1991.
Outward currents activated by depolarization were studied in the neuropilar membrane of locust nonspiking local interneurons, using the single-electrode voltage-clamp technique in situ. Preliminary observation of these currents in 272 neurons revealed two families. The first and most commonly observed (85% of recordings) showed a large transient current followed by a slowly decaying/late current. The second (15% of recordings) showed an additional outward current with a slow rate of activation, a peak within 100-150 msec, and a slow rate of inactivation. Only neurons of the first type were studied further. The transient current was activated by depolarization around -60 mV, with a time to peak of approximately 11 msec at -50 mV and less than 3 msec at -20 mV. This current decayed exponentially, with a time constant of 8.1 +/- 1.6 msec (n = 8 interneurons) at -30 mV. This time constant of inactivation did not appear to depend strongly on membrane voltage, in the range in which it was studied. A second and longer time constant of inactivation of 50-400 msec could not be assigned to either of the transient and late components of the outward current. The ratio of transient-to-late current varied between 1.6 and 5.4, with a mean of about 2.5. The reversal potential for the transient current could, on average, be shifted by 14 mV by a threefold increase in the bath K+ concentration, indicating that K+ is a charge carrier for the current. The transient current became inactivated with maintained depolarization and appeared half-inactivated at about -60 mV (slope factor k1/2 = 8 mV). This current was thus not fully inactivated at "resting" potential (average, -58 mV). Recovery from inactivation followed a single exponential time course, with a time constant of approximately 100 msec at -80 mV. The time course of recovery from inactivation of the transient current was well correlated with that of the recovery of transient outward rectification, as measured in current-clamp recording. Tetraethylammonium, at a bath concentration of 10 mM reduced the transient current by 70% and the delayed current by 60%. 4-Aminopyridine, at a bath concentration of 5 mM, had a significant effect in only two of five interneurons, reducing the transient current by approximately 85% and the late current by approximately 15%. Quinidine at a bath concentration of 100 microM was ineffective. Although these blockers did not allow a clear pharmacological separation of the currents, they were effective in reducing the outward rectification observed in current clamp during step depolarization.(ABSTRACT TRUNCATED AT 400 WORDS)
采用单电极电压钳原位技术,对蝗虫非锋电位局部中间神经元神经纤维网膜中去极化激活的外向电流进行了研究。对272个神经元中这些电流的初步观察显示出两个类型。第一种也是最常见的(85%的记录)显示出一个大的瞬态电流,随后是一个缓慢衰减的/延迟电流。第二种(15%的记录)显示出一个额外的外向电流,其激活速率缓慢,在100 - 150毫秒内达到峰值,且失活速率缓慢。仅对第一种类型的神经元进行了进一步研究。瞬态电流在约 -60 mV的去极化时被激活,在 -50 mV时达到峰值的时间约为11毫秒,在 -20 mV时小于3毫秒。该电流呈指数衰减,在 -30 mV时的时间常数为8.1±1.6毫秒(n = 8个中间神经元)。在研究的膜电压范围内,这种失活时间常数似乎并不强烈依赖于膜电压。无法将50 - 400毫秒的第二个且更长的失活时间常数归因于外向电流的瞬态和延迟成分中的任何一个。瞬态电流与延迟电流的比值在1.6至5.4之间变化,平均值约为2.5。瞬态电流的反转电位平均可因浴槽中K⁺浓度增加三倍而偏移14 mV,表明K⁺是该电流的电荷载体。瞬态电流在持续去极化时会失活,在约 -60 mV时似乎处于半失活状态(斜率因子k1/2 = 8 mV)。因此,该电流在“静息”电位(平均为 -58 mV)时并未完全失活。从失活状态恢复遵循单一指数时间进程,在 -80 mV时时间常数约为100毫秒。瞬态电流从失活状态恢复的时间进程与电流钳记录中测量的瞬态外向整流恢复的时间进程密切相关。浴槽浓度为10 mM的四乙铵使瞬态电流降低了70%,使延迟电流降低了60%。浴槽浓度为5 mM的4 - 氨基吡啶仅在五个中间神经元中的两个中产生了显著作用,使瞬态电流降低了约85%,使延迟电流降低了约15%。浴槽浓度为100 microM的奎尼丁无效。尽管这些阻滞剂无法对电流进行明确的药理学区分,但它们有效地减少了在阶跃去极化期间电流钳中观察到的外向整流。(摘要截断于400字)