Kann Oliver, Kovács Richard
Institut für Neurophysiologie, Charité-Universitätsmedizin Berlin, Tucholskystrasse 2, 10117 Berlin, Germany.
Am J Physiol Cell Physiol. 2007 Feb;292(2):C641-57. doi: 10.1152/ajpcell.00222.2006. Epub 2006 Nov 8.
Mitochondria are central for various cellular processes that include ATP production, intracellular Ca(2+) signaling, and generation of reactive oxygen species. Neurons critically depend on mitochondrial function to establish membrane excitability and to execute the complex processes of neurotransmission and plasticity. While much information about mitochondrial properties is available from studies on isolated mitochondria and dissociated cell cultures, less is known about mitochondrial function in intact neurons in brain tissue. However, a detailed description of the interactions between mitochondrial function, energy metabolism, and neuronal activity is crucial for the understanding of the complex physiological behavior of neurons, as well as the pathophysiology of various neurological diseases. The combination of new fluorescence imaging techniques, electrophysiology, and brain slice preparations provides a powerful tool to study mitochondrial function during neuronal activity, with high spatiotemporal resolution. This review summarizes recent findings on mitochondrial Ca(2+) transport, mitochondrial membrane potential (DeltaPsi(m)), and energy metabolism during neuronal activity. We will first discuss interactions of these parameters for experimental stimulation conditions that can be related to the physiological range. We will then describe how mitochondrial and metabolic dysfunction develops during pathological neuronal activity, focusing on temporal lobe epilepsy and its experimental models. The aim is to illustrate that 1) the structure of the mitochondrial compartment is highly dynamic in neurons, 2) there is a fine-tuned coupling between neuronal activity and mitochondrial function, and 3) mitochondria are of central importance for the complex behavior of neurons.
线粒体对于包括ATP生成、细胞内Ca(2+)信号传导以及活性氧生成在内的各种细胞过程至关重要。神经元严重依赖线粒体功能来建立膜兴奋性，并执行神经传递和可塑性的复杂过程。虽然从对分离的线粒体和离体细胞培养物的研究中可以获得许多关于线粒体特性的信息，但对于脑组织中完整神经元的线粒体功能了解较少。然而，详细描述线粒体功能、能量代谢和神经元活动之间的相互作用对于理解神经元的复杂生理行为以及各种神经疾病的病理生理学至关重要。新的荧光成像技术、电生理学和脑片制备方法的结合提供了一个强大的工具，能够以高时空分辨率研究神经元活动期间的线粒体功能。本综述总结了关于神经元活动期间线粒体Ca(2+)转运、线粒体膜电位（DeltaPsi(m)）和能量代谢的最新发现。我们将首先讨论这些参数在与生理范围相关的实验刺激条件下的相互作用。然后，我们将描述在病理性神经元活动期间线粒体和代谢功能障碍是如何发展的，重点关注颞叶癫痫及其实验模型。目的是说明：1）线粒体区室的结构在神经元中高度动态；2）神经元活动与线粒体功能之间存在精细调节的耦合；3）线粒体对于神经元的复杂行为至关重要。
