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首页> 外文期刊>Journal of Neurophysiology >RINm5f cells express inactivating BK channels whereas HIT cells express noninactivating BK channels.
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RINm5f cells express inactivating BK channels whereas HIT cells express noninactivating BK channels.

机译：RINm5f细胞表达失活的BK通道，而HIT细胞表达失活的BK通道。

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摘要

Large-conductance Ca2+- and voltage-activated BK-type K+ channels are expressed abundantly in normal rat pancreatic islet cells and in the clonal rat insulinoma tumor (RINm5f) and hamster insulinoma tumor (HIT) beta cell lines. Previous work has suggested that the Ca2+ sensitivity of BK channels in RIN cells is substantially less than that in HIT cells, perhaps contributing to differences between the cell lines in responsiveness to glucose in mediating insulin secretion. In both RIN cells and normal pancreatic beta cells, BK channels are thought to play a limited role in responses of beta cells to secretagogues and in the electrical activity of beta cells. Here we examine in detail the properties of BK channels in RIN and HIT cells using inside-out patches and whole cell recordings. BK channels in RIN cells exhibit rapid inactivation that results in an anomalous steady-state Ca2+ dependence of activation. In contrast, BK channels in HIT cells exhibit the more usual noninactivating behavior. When BK inactivation is taken into account, the Ca2+ and voltage dependence of activation of BK channels in RIN and HIT cells is essentially indistinguishable. The properties of BK channel inactivation in RIN cells are similar to those of inactivating BK channels (termed BKi channels) previously identified in rat chromaffin cells. Inactivation involves multiple, trypsin-sensitive cytosolic domains and exhibits a dependence on Ca2+ and voltage that appears to arise from coupling to channel activation. In addition, the rates of inactivation onset and recovery are similar to that of BKi channels in chromaffin cells. The charybdotoxin (CTX) sensitivity of BKi currents is somewhat less than that of the noninactivating BK variant. Action potential voltage-clamp waveforms indicate that BK current is activated only weakly by Ca2+ influx in RIN cells but more strongly activated in HIT cells even when Ca2+ current magnitude is comparable. Concentrations of CTX sufficient to block BKi current in RIN cells have no effect on action potential activity initiated by glucose or DC injection. Despite its abundant expression in RIN cells, BKi current appears to play little role in action potential activity initiated by glucose or DC injection in RIN cells, but BK current may play an important role in action potential repolarization in HIT cells.
机译：大电导的Ca2 +和电压激活的BK型K +通道在正常大鼠胰岛细胞以及克隆大鼠胰岛素瘤肿瘤（RINm5f）和仓鼠胰岛素瘤肿瘤（HIT）β细胞系中大量表达。先前的工作表明，RIN细胞中BK通道的Ca2 +敏感性大大低于HIT细胞，这可能是细胞系之间介导胰岛素分泌对葡萄糖反应性差异的原因。在RIN细胞和正常胰腺β细胞中，BK通道被认为在β细胞对促分泌素的反应以及β细胞的电活动中起有限的作用。在这里，我们使用从里到外的贴片和整个细胞记录详细检查RIN和HIT细胞中BK通道的特性。 RIN细胞中的BK通道表现出快速失活，从而导致异常的稳态Ca2 +依赖性激活。相反，HIT细胞中的BK通道表现出更常见的非灭活行为。当考虑到BK灭活时，RIN和HIT细胞中BK通道激活的Ca2 +和电压依赖性基本上是无法区分的。 RIN细胞中BK通道失活的特性与先前在大鼠嗜铬细胞中鉴定出的BK通道失活（称为BKi通道）相似。失活涉及多个胰蛋白酶敏感的胞质结构域，并表现出对Ca2 +和电压的依赖性，而Ca2 +和电压似乎是由于与通道激活偶联而产生的。另外，灭活的开始和恢复的速率与嗜铬细胞中的BKi通道相似。 BKi电流的炭疽毒素（CTX）敏感性略低于非灭活性BK变体。动作电位电压钳位波形表明，即使在Ca2 +电流大小相当的情况下，RIN细胞中Ca2 +的流入也只能弱激活BK电流，而在HIT细胞中，BK电流才可以被强激活。足以阻断RIN细胞中BKi电流的CTX浓度对葡萄糖或DC注射引发的动作电位活性没有影响。尽管在RIN细胞中有大量表达，但BKi电流在RIN细胞中葡萄糖或DC注入引发的动作电位活性中似乎起着很小的作用，但是BK电流可能在HIT细胞的动作电位复极化中起重要作用。

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