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超短电刺激对细胞内 Ca2+的募集:脉宽的影响。

Recruitment of the intracellular Ca2+ by ultrashort electric stimuli: the impact of pulse duration.

机构信息

Frank Reidy Research Center for Bioelectrics, Old Dominion University, Norfolk, VA 23508, USA.

出版信息

Cell Calcium. 2013 Sep;54(3):145-50. doi: 10.1016/j.ceca.2013.05.008. Epub 2013 Jun 15.

Abstract

Nanosecond-duration electric stimuli are distinguished by the ability to permeabilize intracellular membranes and recruit Ca2+ from intracellular stores. We quantified this effect in non-excitable cells (CHO) using ratiometric Ca2+ imaging with Fura-2. In a Ca(2+)-free medium, 10-, 60-, and 300-ns stimuli evoked Ca2+ transients by mobilization of Ca2+ from the endoplasmic reticulum. With 2 mM external Ca2+, the transients included both extra- and intracellular components. The recruitment of intracellular Ca2+ increased as the stimulus duration decreased. At the threshold of 200-300 nM, the transients were amplified by calcium-induced calcium release. We conclude that nanosecond stimuli mimic Ca2+ signaling while bypassing the usual receptor- and channels-mediated cascades. The recruitment of the intracellular Ca2+ can be controlled by the duration of the stimulus.

摘要

纳秒时长的电刺激具有穿透细胞内膜并从细胞内储存库中募集 Ca2+的能力。我们使用 Fura-2 的比率 Ca2+成像在非兴奋细胞(CHO)中定量了这种效应。在不含 Ca2+的培养基中,10、60 和 300 纳秒的刺激通过从内质网中动员 Ca2+来引发 Ca2+瞬变。在 2 mM 外部 Ca2+下,瞬变包括细胞外和细胞内成分。随着刺激持续时间的减少,细胞内 Ca2+的募集增加。在 200-300 nM 的阈值下,瞬变被钙诱导的钙释放放大。我们得出结论,纳秒刺激模拟了 Ca2+信号转导,同时绕过了通常的受体和通道介导的级联反应。细胞内 Ca2+的募集可以通过刺激的持续时间来控制。

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