Stepanova I V, Kostiuk P H, Kostiuk O P
Fiziol Zh (1994). 2005;51(1):19-25.
We studied the dynamic contribution of endoplasmic reticulum and mitochondria to depolarization-induced Ca2+ transients in small (18-24 microm) DRG neurons of rats. We have used the application of 10 microM of mitochondrial protonophore CCCP for switching off the calcium uptake by mitochondrial uniporter. For depletion of the store of endoplasmic reticulum we applied 1 microM of thapsigargin. Depolarization-induced transients in control conditions and in conditions when one of the mechanisms (mitochondria or endoplasmic reticulum) does not participate in the forming of the shape of Ca2+ transient have been studied. This allowed us to clarify the kinetics of mitochondrial and endoplasmic reticulum uptake and release of calcium in the process of the neuronal activity. We have determined the main characteristics of functioning of above-named calcium stores in the process of cell excitation, such as time of the beginning of uptake, time and duration of maximum activity etc. We concluded, that mitochondria and endoplasmic reticulum are acting in opposite directions at least in the phase of the beginning of the transient. Mitochondria are limiting the amplitude of the transient during depolarization, at the same time the endoplasmic reticulum is increasing the amplitude of the transient by CICR (calcium-induced calcium release) mechanism. Mitochondria store calcium released from endoplasmic reticulum by application of 30 mM caffeine. Inhibition of the mitochondrial uniporter results in reduction of amplitude of repetitive caffeine application compared with control conditions. We have compared the kinetics of mitochondrial participation in the formation of calcium signal when the initial sources of calcium ions were different. Our results allow us to suggest a close functional dynamic interactions between mitochondria and endoplasmic reticulum during calcium signaling in sensory neurons.
我们研究了内质网和线粒体对大鼠小直径（18 - 24微米）背根神经节（DRG）神经元去极化诱导的Ca2+瞬变的动态作用。我们使用10微摩尔的线粒体质子载体羰基氰化物间氯苯腙（CCCP）来关闭线粒体单向转运体的钙摄取。为了耗尽内质网的钙储存，我们应用了1微摩尔的毒胡萝卜素。我们研究了在对照条件下以及当其中一种机制（线粒体或内质网）不参与Ca2+瞬变形状形成的条件下去极化诱导的瞬变。这使我们能够阐明在神经元活动过程中线粒体和内质网摄取和释放钙的动力学。我们确定了上述钙库在细胞兴奋过程中的主要功能特征，如摄取开始时间、最大活性时间和持续时间等。我们得出结论，至少在瞬变开始阶段，线粒体和内质网的作用方向相反。在去极化过程中，线粒体限制瞬变的幅度，同时内质网通过钙诱导钙释放（CICR）机制增加瞬变的幅度。通过应用30毫摩尔咖啡因，线粒体储存从内质网释放的钙。与对照条件相比，抑制线粒体单向转运体会导致重复应用咖啡因时幅度降低。当钙离子的初始来源不同时，我们比较了线粒体参与钙信号形成的动力学。我们的结果使我们能够提出在感觉神经元钙信号传导过程中线粒体和内质网之间存在密切的功能动态相互作用。
