Evidence for voltage-activated outward currents in the neuropilar membrane of locust nonspiking local interneurons

Evidence for voltage-activated outward currents in the neuropilar membrane of locust nonspiking local interneurons
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蝗虫非尖峰局部中间神经元的神经毛膜中电压激活的外向电流的证据

DOI:
10.1523/jneurosci.11-06-01713.1991
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发表时间:
1991
期刊:
The Journal of experimental biology
影响因子:
--
通讯作者:
G. Laurent
G. Laurent
中科院分区:
--
文献类型:
--
作者:
G. Laurent

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利用原位单电极电压钳技术,研究了蝗虫局部非尖峰中间神经元的神经柱膜中去极化激活的外向电流。对272个神经元电流的初步观察揭示了两个家族。第一个也是最常观察到的(85%的记录)显示一个大的瞬态电流,然后是一个缓慢衰减/延迟电流。第二个(15%的记录)显示了一个额外的外向电流,激活速度慢,在100-150毫秒内达到峰值,并且失活速度慢。仅对第一类神经元进行了进一步的研究。瞬态电流在-60 mV左右被去极化激活,在-50 mV时达到峰值的时间约为11毫秒,在-20 mV时不到3毫秒。该电流在-30 mV时呈指数衰减,时间常数为8.1 +/- 1.6 msec (n = 8个中间神经元)。在研究的范围内,这种失活时间常数似乎并不强烈依赖于膜电压。一秒或更长的失活时间常数为50-400毫秒,不能分配给向外电流的瞬态和后期分量。暂态电流与后期电流之比在1.6 ~ 5.4之间变化,平均值约为2.5。当溶液中K+浓度增加三倍时,瞬态电流的反转电位平均可以移动14 mV,这表明K+是电流的电荷载体。暂态电流在持续去极化的情况下失活,在-60 mV左右(斜率系数k1/2 = 8 mV)呈现半失活状态。因此,该电流在“静息”电位(平均-58 mV)下没有完全灭活。失活后的恢复遵循单指数时间过程,在-80 mV时时间常数约为100毫秒。从暂态电流失活恢复的时间过程与瞬态外向整流恢复的时间过程有很好的相关性,这是在电流钳记录中测量到的。四乙基铵溶液浓度为10 mM时,瞬态电流降低70%,延迟电流降低60%。4-氨基吡啶在溶液浓度为5 mM时,仅对5个中间神经元中的2个有显著影响,使瞬时电流减少约85%,后期电流减少约15%。奎尼丁在浴液浓度为100微米时无效。虽然这些阻滞剂不允许电流的明确药理学分离,但它们有效地减少了在步骤去极化期间在电流钳中观察到的向外整流。
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.
DOI: 10.1126/science.2333511
发表时间: 1990-05
期刊: Science
影响因子: 56.9
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影响因子: 2.5
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发表时间: 1982
期刊: Science (New York, N.Y.)
影响因子: --
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影响因子: 2.5
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