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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Mitochondrial calcium ion and membrane potential transients follow the pattern of epileptiform discharges in hippocampal slice cultures.
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Mitochondrial calcium ion and membrane potential transients follow the pattern of epileptiform discharges in hippocampal slice cultures.

机译：线粒体钙离子和膜电位瞬变遵循海马切片培养物中癫痫样放电的模式。

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Emerging evidence suggests that mitochondrial dysfunction contributes to the pathophysiology of epilepsy. Recurrent mitochondrial Ca2+ ion load during seizures might act on mitochondrial membrane potential (DeltaPsim) and proton motive force. By using electrophysiology and confocal laser-scanning microscopy, we investigated the effects of epileptiform activity, as induced by low-Mg2+ ion perfusion in hippocampal slice cultures, on changes in DeltaPsim and in mitochondrial Ca2+ ion concentration ([Ca2+]m). The mitochondrial compartment was identified by monitoring DeltaPsim in the soma and dendrites of patched CA3 pyramidal cells using the mitochondria-specific voltage-sensitive dye rhodamine-123 (Rh-123). Interictal activity was accompanied by localized mitochondrial depolarization that was restricted to a few mitochondria in small dendrites. In contrast, robust Rh-123 release into the cytosol was observed during seizure-like events (SLEs), indicating simultaneous depolarization of mitochondria. This was critically dependent on Ca2+ ion uptake and extrusion, because inhibition of the mitochondrial Ca2+ ion uniporter by Ru360 and the mitochondrial Na+/Ca2+ ion exchanger by 7-chloro-5-(2-chlorophenyl)-1,5-dihydro-4,1-benzothiazepin-2(3H)-one but not the inhibitor of mitochondrial permeability transition pore, cyclosporin A, decreased the SLE-associated mitochondrial depolarization. The Ca2+ ion dependence of simultaneous mitochondrial depolarization suggested enhanced Ca2+ ion cycling across mitochondrial membranes during epileptiform activity. Indeed, [Ca2+]m fluctuated during interictal activity in single dendrites, and these fluctuations spread over the entire mitochondrial compartment during SLEs, as revealed using mitochondria-specific dyes (rhod-2 and rhod-ff) and spatial frequency-based image analysis. These findings strengthen the hypothesis that epileptic activity results in Ca2+ ion-dependent changes in mitochondrial function that might contribute to the neuronal injury during epilepsy.
机译：越来越多的证据表明线粒体功能障碍与癫痫的病理生理有关。癫痫发作中反复出现的线粒体Ca2 +离子负荷可能作用于线粒体膜电位（DeltaPsim）和质子动力。通过使用电生理学和共聚焦激光扫描显微镜，我们研究了海马切片培养物中低Mg2 +离子灌注引起的癫痫样活性对DeltaPsim和线粒体Ca2 +离子浓度（[Ca2 +] m）变化的影响。线粒体区室通过使用线粒体特异性电压敏感染料若丹明-123（Rh-123）监测体细胞和修补的CA3锥体细胞的树突来识别线粒体。间隔间的活动伴随着局部线粒体去极化，其局限于小树突中的少数线粒体。相反，在癫痫样事件（SLE）期间观察到Rh-123强烈释放到细胞质中，表明线粒体同时去极化。这主要取决于Ca2 +离子的吸收和挤出，因为Ru360抑制了线粒体Ca2 +离子单向转运，而7-氯-5-（2-氯苯基）-1,5-二氢-4抑制了线粒体Na + / Ca2 +离子交换剂， 1-苯并噻唑-2-2（3H）-但不是线粒体通透性过渡孔抑制剂环孢菌素A减少了SLE相关的线粒体去极化。线粒体同时去极化的Ca2 +离子依赖性表明癫痫样活动期间跨线粒体膜的Ca2 +离子循环增强。确实，[Ca2 +] m在单个树突的间质活动期间会波动，并且这些波动会在SLE期间散布到整个线粒体区室，如使用线粒体特异性染料（rhod-2和rhod-ff）和基于空间频率的图像分析所揭示的。这些发现加强了以下假设：癫痫活动会导致线粒体功能中Ca2 +离子依赖性变化，这可能会导致癫痫期间的神经元损伤。

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