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首页> 外文期刊>The European Journal of Neuroscience >Ca2+ signalling and changes of mitochondrial function during low-Mg2+-induced epileptiform activity in organotypic hippocampal slice cultures.
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Ca2+ signalling and changes of mitochondrial function during low-Mg2+-induced epileptiform activity in organotypic hippocampal slice cultures.

机译：Ca2 +信号传导和低Mg2 +诱导的癫痫样海马切片培养物中的癫痫样活动期间线粒体功能的变化。

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摘要

Several lines of evidence indicate that augmented neuronal activity is associated with increased mitochondrial function, however, the mechanisms of coupling are still unclear. In this study we used a low extracellular Mg2+ concentration and short stimulus trains to evoke neuronal hyperactivity in the form of seizure-like events (SLE) in hippocampal slice cultures. Simultaneous microfluorimetric and electrophysiological techniques were applied to gain insight into changes of Ca2+ concentration in different compartments and into mitochondrial function. SLEs were associated with a large decrease of the extracellular Ca2+ concentration ([Ca2+]e), a spiking increase of the cytoplasmic and a smoothed elevation of the mitochondrial Ca2+ concentration (cytoplasmic concentration [Ca2+]i; intramitrochondrial concentration [Ca2+]m). Following an initial apparent decline in the mitochondrial membrane potential (DeltaPsi) and NAD(P)H autofluorescence, mitochondria depolarized and NADH production was augmented. Furthermore, SLEs were associated with increased oxidation of dihydroethidine (HEt). Our data suggest that intramitochondrial Ca2+ accumulation stimulates NADH production and production of radical oxygen species (ROS). Interestingly, mitochondrial depolarization followed [Ca2+]i and [Ca2+]m changes with a delay implying that electrogenic extrusion of Ca2+ from the mitochondrial matrix might be responsible for the depolarization of the mitochondrial membrane.
机译：几条证据表明，神经元活性的增强与线粒体功能的增强有关，但是，耦合机制仍不清楚。在这项研究中，我们使用了低的细胞外Mg2 +浓度和短的刺激训练，以海马切片培养物中癫痫样事件（SLE）的形式引起神经元过度活跃。同时使用微荧光和电生理技术来了解不同隔室中Ca2 +浓度的变化以及线粒体功能。 SLE与细胞外Ca2 +浓度（[Ca2 +] e）的大幅降低，细胞质的突增和线粒体Ca2 +浓度（细胞质浓度[Ca2 +] i;线粒体内浓度[Ca2 +] m）的升高有关。线粒体膜电位（DeltaPsi）和NAD（P）H自发荧光最初出现明显下降后，线粒体去极化，NADH产量增加。此外，SLE与二氢乙啶（HEt）的氧化增加有关。我们的数据表明线粒体内Ca2 +的积累会刺激NADH的产生和自由基氧（ROS）的产生。有趣的是，线粒体去极化随[Ca2 +] i和[Ca2 +] m的变化而延迟，这暗示着从线粒体基质中电生的Ca2 +挤出可能导致线粒体膜的去极化。

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