Gibson G E, Nielsen P, Toral-Barza L
Cornell University Medical College, Burke Medical Research Institute, White Plains, NY 10605.
Neurosci Lett. 1992 Apr 13;138(1):133-6. doi: 10.1016/0304-3940(92)90489-t.
The precise mechanism by which altered oxidative metabolism impairs neuronal function is unknown. Previous indirect studies suggest that anoxia's effects on the mitochondrial membrane potentials may underlie anoxia's actions. Twenty minutes of anoxia reduced the mitochondrial membrane potential of intact synaptosomes by 38-59 mV, but diminished the plasma membrane potential by only 4-10 mV. Anoxia did not alter the response of the plasma or mitochondrial membrane potentials to K+, nor did anoxia affect the reaction of the plasma membrane potential to valinomycin. However, anoxia diminished the response of the mitochondrial membrane potential to valinomycin by 50%. Thus, partial collapse of the mitochondrial membrane potential may be an important mediator of hypoxia-or anoxia-induced changes in neuronal function.
氧化代谢改变损害神经元功能的确切机制尚不清楚。先前的间接研究表明，缺氧对线粒体膜电位的影响可能是缺氧作用的基础。20分钟的缺氧使完整突触体的线粒体膜电位降低38 - 59 mV，但仅使质膜电位降低4 - 10 mV。缺氧并未改变质膜或线粒体膜电位对钾离子的反应，也不影响质膜电位对缬氨霉素的反应。然而，缺氧使线粒体膜电位对缬氨霉素的反应降低了50%。因此，线粒体膜电位的部分崩溃可能是缺氧或无氧诱导的神经元功能变化的重要介质。
