Characterization of outward currents in neurons of the avian nucleus magnocellularis
Characterization of outward currents in neurons of the avian nucleus magnocellularis
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DOI：
10.1152/jn.1998.80.6.2824
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发表时间：
1998-12-01
影响因子：
2.5
通讯作者：
Trussell, L
中科院分区：
文献类型：
--
作者：
Rathouz, M;Trussell, L
大细胞核（NM）的神经元通过各种电压门控离子通道和配体门控离子通道的汇聚来保留听觉信号的时序。为了更好地了解这些通道如何相互作用，我们对脑切片中 NM 神经元的外向电流的动力学、电压敏感性和药理学进行了表征。正如钾所携带的电流所预期的那样，外向电流的反转电位 (E-rev) 随钾浓度的变化而变化。然而，E-rev 始终比钾的能斯特电位 (E-K) 更正。E-rev 与计算的 E-K 的偏差很可能是由于静息和去极化步骤期间活跃的钾电导导致细胞外空间中钾的积累引起的。研究了电压和药理学敏感性不同的三种外向钾电流。四乙铵 (TEA) 敏感的高阈值电流在去极化开始后 1-5 ms 内被激活，半最大激活电压 (V-1/2) 为 -19 mV。它被 4-氨基吡啶 (4-AP) 部分阻断，是 NM 神经元的主要离子电导。树突毒素-I (DTX) 和 4-AP 敏感、低阈值电流的 V-1/2 为 -58 mV、快速激活动力学、仅部分失活，衰减时间常数在 20 至 100 ms 之间。观察到快速失活电流，该电流对 TEA 和 DTX 具有抗性，并被细胞内 Cs+ 阻断。瞬态电流在静息电位下几乎完全失活。当电位对引起激活的电位呈负值时，失活的发生最快。当细胞内的K+被Cs'取代时。获得了大的向内和向外电流，分别对应于上述DTX和TEA敏感电流。向外，TEA 敏感电流由 Cs+ 承载，P-Cs/P-K 接近 0.1。在电流钳位的神经元中，DTX 诱导重复放电并增加接近静止状态的膜时间常数，但对动作电位持续时间几乎没有影响。这些研究表明，低阈值、DTX 敏感电流在使 NM 神经元对突触刺激的开始和消失高度敏感方面发挥着关键作用。
Neurons of the nucleus magnocellularis (NM) preserve the timing of auditory signals through the convergence of a variety of voltage- and ligand-gated ion channels. To understand better how these channels interact, we have characterized the kinetics, voltage sensitivity, and pharmacology of outward currents of NM neurons in brain slices. The reversal potential (E-rev) of outward currents varied with potassium concentration as expected for currents carried by potassium. However, E-rev was consistently more positive than the Nernst potential for potassium (E-K) Deviation of E-rev from the calculated E-K most likely arose from potassium accumulation in extracellular spaces by potassium conductances active at rest and during depolarizing steps. Three outward potassium currents were studied that varied in voltage and pharmacological sensitivity. A tetraethylammonium (TEA)-sensitive, high-threshold current was activated within 1-5 ms of the onset of depolarization, with a half-maximal activation voltage (V-1/2) Of -19 mV. It was blocked partially by 4-aminopyridine (4-AP) and was the dominant ionic conductance of NM neurons. A dendrotoxin-I (DTX) and 4-AP-sensitive, low-threshold current had a V-1/2 of -58 mV, rapid activation kinetics, and only partial inactivation, with decay time constants between 20 and 100 ms. A rapidly inactivating current was observed that was resistant to TEA and DTX and was blocked by intracellular Cs+. The transient current was inactivated almost completely at the resting potential. The onset of inactivation was fastest at potentials negative to those that caused activation. When intracellular K+ was replaced by Cs'. large inward and outward currents were obtained that corresponded respectively to the above-mentioned DTX- and TEA-sensitive currents. Outward, TEA-sensitive current was carried by Cs+, with a P-Cs/P-K of similar to 0.1. In current-clamped neurons, DTX induced repetitive firing and increased membrane time constant near rest but had little effect on action potential duration. These studies indicate that a low-threshold, DTX-sensitive current plays a key role in making NM neurons highly responsive to the onset and offset of synaptic stimuli.