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首页> 外文期刊>American Journal of Physiology >Role of domain calcium in purinergic P2X2 receptor channel desensitization
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Role of domain calcium in purinergic P2X2 receptor channel desensitization

机译：域钙在嘌呤能P2X2受体通道脱敏中的作用

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摘要

Activation of P2X2 receptor channels (P2X2Rs) is characterized by a rapid current growth accompanied by a decay of current during sustained ATP application, a phenomenon known as receptor desensitization. Using rat, mouse, and human receptors, we show here that two processes contribute to receptor desensitization: bath calcium-independent desensitization and calcium-dependent desensitization. Calcium-independent desensitization is minor and comparable during repetitive agonist application in cells expressing the full size of the receptor but is pronounced in cells expressing shorter versions of receptors, indicating a role of the COOH terminus in control of receptor desensitization. Calcium-dependent desensitization is substantial during initial agonist application and progressively increases during repetitive agonist application in bath ATP and calcium concentration-dependent manners. Experiments with substitution of bath Na+ with 7V-methyl-D-glucamine (NMDG+), a large organic cation, indicate that receptor pore dilation is a calcium-independent process in contrast to receptor desensitization. A decrease in the driving force for calcium by changing the holding potential from —60 to +120 mV further indicates that calcium influx through the channel pores at least partially accounts for receptor desensitization. Experiments with various receptor chimeras also indicate that the transmembrane and/or intracellular domains of P2X2R are required for development of calcium-dependent desensitization and that a decrease in the amplitude of current slows receptor desensitization. Simultaneous calcium and current recording shows development of calcium-dependent desensitization without an increase in global intracellular calcium concentrations. Combined with experiments with clamping intrapipette concentrations of calcium at various levels, these experiments indicate that domain calcium is sufficient to establish calcium-dependent receptor desensitization in experiments with whole-cell recordings.
机译：P2X2受体通道的激活（P2X2RS）的特征在于通过持续的ATP应用期间的电流衰减的快速流动生长，该现象称为受体脱敏。使用大鼠，小鼠和人类受体，我们在此显示出两种方法有助于受体脱敏：浴钙无关的脱敏和钙依赖性脱敏。钙无关的脱敏在表达受体的全尺寸的细胞中的重复激动剂施用期间，但在表达较短版本的受体中的细胞中，表明COOH末端对受体脱敏的作用的作用。钙依赖性脱敏在初始激动剂施用期间是显着的，并且在浴ATP和钙浓度依赖的举射中的重复激动剂应用过程中逐渐增加。用7V-甲基-D-葡聚糖（NMDG +）取代浴Na +的实验，该大量有机阳离子表明受体孔隙扩张是与受体脱敏相反的钙无关的方法。通过从-60至+120mV改变保持电位的钙的驱动力的减小进一步表明通过通道孔隙孔孔至少部分地估计受体脱敏。具有各种受体嵌合体的实验还表明，P2X2R的跨膜和/或细胞内域是钙依赖性脱敏的发展，并且电流幅度的减小减慢受体脱敏。同时钙和电流记录显示钙依赖性脱敏的发展，而不会增加全球细胞内钙浓度。结合在各种水平夹持钙的钙脊柱管浓度的实验，这些实验表明，结构域钙足以建立依赖于全细胞记录的实验中的钙依赖受体脱敏。

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