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首页> 外文期刊>The Journal of general physiology >Influence of sodium-calcium exchange on calcium current rundown and the duration of calcium-dependent chloride currents in pituitary cells, studied with whole cell and perforated patch recording.
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Influence of sodium-calcium exchange on calcium current rundown and the duration of calcium-dependent chloride currents in pituitary cells, studied with whole cell and perforated patch recording.

机译：钠钙交换对垂体细胞钙电流减少和钙依赖性氯离子电流持续时间的影响，已通过全细胞和穿孔膜片记录研究。

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The whole cell patch-clamp technique, in both standard and perforated patch configurations, was used to study the influence of Na+-Ca++ exchange on rundown of voltage-gated Ca++ currents and on the duration of tail currents mediated by Ca++-dependent Cl- channels. Ca++ currents were studied in GH3 pituitary cells; Ca++-dependent Cl- currents were studied in AtT-20 pituitary cells. Na+-Ca++ exchange was inhibited by substitution of tetraethylammonium (TEA+) or tetramethylammonium (TMA+) for extracellular Na+. Control experiments demonstrated that substitution of TEA+ for Na+ did not produce its effects via a direct interaction with Ca++-dependent Cl- channels or via blockade of Na+-H+ exchange. When studied with standard whole cell methods, Ca++ and Ca++-dependent Cl- currents ran down within 5-20 min. Rundown was accelerated by inhibition of Na+-Ca++ exchange. In contrast, the amplitude of both Ca++ and Ca++-dependent Cl- currents remained stable for 30-150 min when the perforated patch method was used. Inhibition of Na+-Ca++ exchange within the first 30 min of perforated patch recording did not cause rundown. The rate of Ca++-dependent Cl- current deactivation also remained stable for up to 70 min in perforated patch experiments, which suggests that endogenous Ca++ buffering mechanisms remained stable. The duration of Ca++-dependent Cl- currents was positively correlated with the amount of Ca++ influx through voltage-gated Ca++ channels, and was prolonged by inhibition of Na+-Ca++ exchange. The influence of Na+-Ca++ exchange on Cl- currents was greater for larger currents, which were produced by greater influx of Ca++. Regardless of Ca++ influx, however, the prolongation of Cl- tail currents that resulted from inhibition of Na+-Ca++ exchange was modest. Tail currents were prolonged within tens to hundreds of milliseconds of switching from Na+- to TEA+-containing bath solutions. After inhibition of Na+-Ca++ exchange, tail current decay kinetics remained complex. These data strongly suggest that in the intact cell, Na+-Ca++ exchange plays a direct but nonexclusive role in limiting the duration of Ca++-dependent membrane currents. In addition, these studies suggest that the perforated patch technique is a useful method for studying the regulation of functionally relevant Ca++ transients near the cytoplasmic surface of the plasma membrane.
机译：使用全细胞膜片钳技术，在标准膜片和穿孔膜片配置中，都用于研究Na + -Ca ++交换对电压门控Ca ++电流的下调以及由依赖Ca ++的Cl-通道介导的尾电流持续时间的影响。在GH3垂体细胞中研究了Ca ++电流;在AtT-20垂体细胞中研究了依赖Ca ++的Cl-电流。通过用四乙铵（TEA +）或四甲铵（TMA +）替代细胞外Na +，可以抑制Na + -Ca ++交换。对照实验表明，TEA +取代Na +不会通过与依赖Ca ++的Cl-通道直接相互作用或通过阻断Na + -H +交换而产生其作用。用标准的全细胞方法研究时，Ca ++和依赖Ca ++的Cl电流在5-20分钟内下降。通过抑制Na + -Ca ++交换，加速了流失。相反，当使用穿孔贴片方法时，Ca ++和依赖Ca ++的Cl电流的幅度在30-150分钟内保持稳定。在穿孔补丁记录的前30分钟内，Na + -Ca ++交换的抑制不会导致流失。在穿孔斑贴实验中，Ca ++依赖的Cl电流失活的速率在长达70分钟的时间内也保持稳定，这表明内源Ca ++缓冲机制保持稳定。依赖Ca ++的Cl电流的持续时间与通过电压门控的Ca ++通道流入的Ca ++数量呈正相关，并通过抑制Na + -Ca ++交换而延长。对于较大的电流，Na + -Ca ++交换对Cl-电流的影响更大，这是由于Ca ++的大量涌入而产生的。但是，不管Ca ++的涌入如何，由于抑制Na + -Ca ++交换而导致的Cl-尾电流的延长是适度的。从含Na +到TEA +的浴液转换，尾电流在数十到数百毫秒内延长。抑制Na + -Ca ++交换后，尾电流衰减动力学仍然很复杂。这些数据强烈表明，在完整细胞中，Na + -Ca ++交换在限制Ca ++依赖性膜电流持续时间方面起着直接但非排他的作用。此外，这些研究表明，穿孔膜片技术是研究质膜细胞质表面附近功能相关的Ca ++瞬变调控的有用方法。

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