Mechanism of generation of spontaneous miniature outward currents (SMOCs) in retinal amacrine cells.
Mechanism of generation of spontaneous miniature outward currents (SMOCs) in retinal amacrine cells.
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DOI：
10.1085/jgp.20028478
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发表时间：
2002-04
期刊：
影响因子：
--
通讯作者：
Slaughter MM
中科院分区：
文献类型：
--
作者：
Mitra P;Slaughter MM
视网膜无长突细胞的一个亚型表现出独特的 K+ 电流阵列。在-60至-40 mV的窄电压范围内观察到自发微型外向电流（SMOC）。大约-40 mV 以上的去极化与 SMOC 的消失以及瞬态 (Ito) 和持续 (Iso) 外向 K+ 电流的出现有关。 Ito 出现在约 -40 mV 处，其表观幅度随电压呈双相，而 Iso 出现在 -30 mV 附近并线性增加。 SMOC、Ito 和 Iso 的一个组成部分是 Ca2+ 依赖性的。 SMOC 呈尖峰状，随机发生，并且衰减时间明显长于达到峰值的时间。在存在镉或钴的情况下，可以在 -20 mV 及以上的电压下产生具有与正常林格氏液相同的药理特性的 SMOC。它们的平均振幅相对于 [K+]ext 是能斯特式的，并且被四乙铵阻断。 SMOC 受伊比利亚毒素抑制，对 apamin 不敏感，并被名义上不含 Ca2+ 的溶液消除，表明存在 BK 型 Ca2+ 激活的 K+ 电流。二氢吡啶 Ca2+ 通道拮抗剂和激动剂分别降低和增加 SMOC 频率。 Ca2+ 通过红藻氨酸受体的渗透没有影响。用兰尼碱阻断细胞器 Ca2+ 通道，或用咖啡因耗尽细胞内 Ca2+ 储备，从而根除 SMOC。 10 mM BAPTA 的内部 Ca2+ 螯合消除了 SMOC，而 10 mM EGTA 则没有效果。这些结果表明了一种机制，即Ca2+通过L型Ca2+通道流入，随后通过兰尼丁受体通过Ca2+诱导的Ca2+释放而放大，导致内部Ca2+局部升高。这种放大的 Ca2+ 信号反过来以不连续的方式激活 BK 通道，从而导致随机出现的 SMOC。
A subtype of retinal amacrine cells displayed a distinctive array of K+ currents. Spontaneous miniature outward currents (SMOCs) were observed in the narrow voltage range of −60 to −40 mV. Depolarizations above approximately −40 mV were associated with the disappearance of SMOCs and the appearance of transient (Ito) and sustained (Iso) outward K+ currents. Ito appeared at about −40 mV and its apparent magnitude was biphasic with voltage, whereas Iso appeared near −30 mV and increased linearly. SMOCs, Ito, and a component of Iso were Ca2+ dependent. SMOCs were spike shaped, occurred randomly, and had decay times appreciably longer than the time to peak. In the presence of cadmium or cobalt, SMOCs with pharmacologic properties identical to those seen in normal Ringer's could be generated at voltages of −20 mV and above. Their mean amplitude was Nernstian with respect to [K+]ext and they were blocked by tetraethylammonium. SMOCs were inhibited by iberiotoxin, were insensitive to apamin, and eliminated by nominally Ca2+-free solutions, indicative of BK-type Ca2+-activated K+ currents. Dihydropyridine Ca2+ channel antagonists and agonists decreased and increased SMOC frequencies, respectively. Ca2+ permeation through the kainic acid receptor had no effect. Blockade of organelle Ca2+ channels by ryanodine, or intracellular Ca2+ store depletion with caffeine, eradicated SMOCs. Internal Ca2+ chelation with 10 mM BAPTA eliminated SMOCs, whereas 10 mM EGTA had no effect. These results suggest a mechanism whereby Ca2+ influx through L-type Ca2+ channels and its subsequent amplification by Ca2+-induced Ca2+ release via the ryanodine receptor leads to a localized elevation of internal Ca2+. This amplified Ca2+ signal in turn activates BK channels in a discontinuous fashion, resulting in randomly occurring SMOCs.
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