对咖啡因敏感的阳离子通道和钙储存的激活和脱敏对水蛭P神经元的电生理特性没有持久的影响

Barbara Sieks, Peter Hochstrate, Wolf-Rüdiger Schlue
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引用次数: 1

摘要

在水蛭P神经元中,咖啡因激活质膜上的非选择性离子通道并诱导细胞内Ca2+释放(Schoppe, J., Hochstrate, P., Schlue, w.r。, 1997年。咖啡因介导水蛭P神经元的阳离子内流和细胞内Ca2+释放。细胞钙22,385-397)。这些影响只在第一次接触咖啡因时突出,而随后的应用基本上无效;即质膜通道和细胞内Ca2+释放机制都不可逆地脱敏。为了研究这种脱敏是否与细胞电生理参数的不可逆变化相平行,我们研究了咖啡因对膜电位和胞质游离Ca2+浓度变化的作用,这些变化是通过改变细胞外液的离子组成或应用5-羟色胺引起的。静息值和任何实验诱导的膜电位或胞质Ca2+浓度的变化都不受咖啡因的影响,这强烈表明,咖啡因敏感离子通道和Ca2+储存的激活和/或脱敏对相关的电化学梯度、膜电导或运输机制没有持久的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Activation and desensitization of the caffeine-sensitive cation channels and calcium stores have no persistent effect on the electrophysiological properties of leech P neurones

In leech P neurones caffeine activates unselective ion channels in the plasma membrane and induces intracellular Ca2+ release (Schoppe, J., Hochstrate, P., Schlue, W.-R., 1997. Caffeine mediates cation influx and intracellular Ca2+ release in leech P neurones. Cell Calcium 22, 385–397). These effects are prominent only upon the first caffeine exposure, while subsequent applications are largely ineffective; i.e. both plasma membrane channels and intracellular Ca2+ release mechanism desensitize irreversibly. In order to examine whether this desensitization is paralleled by irreversible changes in the electrophysiological parameters of the cells, we investigated the action of caffeine on changes in membrane potential and the cytosolic free Ca2+ concentration, which were induced by varying the ionic composition of the extracellular fluid or by application of 5-hydroxytryptamine. Neither the resting values nor any of the experimentally induced shifts in membrane potential or cytosolic Ca2+ concentration were affected by caffeine, which suggests strongly that activation and/or desensitization of the caffeine-sensitive ion channels and Ca2+ stores have no long-lasting effect on the relevant electrochemical gradients, membrane conductances, or transport mechanisms.

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