Verity M A, Brown W J, Cheung M K
Neurochem Res. 1983 Feb;8(2):159-66. doi: 10.1007/BF00963916.
Studies on synaptosome mitochondrial respiration are complicated by "free" mitochondria. Veratridine stimulation of synaptosomal respiration was due to increased Na+ cycling at the synaptosome membrane associated with increased oxidative phosphorylation of intraterminal ADP and was inhibited by oligomycin, ouabain or Na+ free medium. Atractylate or carboxyatractyloside failed to block veratridine-stimulated respiration but inhibited exogenous-ADP-stimulated respiration. Protein synthesis in the synaptosome fraction was inhibited by oligomycin, valinomycin or 2,4-dinitrophenol but was unaffected by excess atractylate. No change in synaptosomal adenine nucleotide content was found in the presence of atractylate, although a significant decrease in the [ATP]/[ADP] was found with oligomycin, veratridine or valinomycin. These findings show that atractylate does not modify intraterminal mitochondrial energy transduction and indirectly suggest an impermeability of the synaptosome membrane to atractylate.
对突触体线粒体呼吸的研究因“游离”线粒体而变得复杂。藜芦碱刺激突触体呼吸是由于突触体膜上Na⁺循环增加，这与终末内ADP的氧化磷酸化增加有关，并且被寡霉素、哇巴因或无Na⁺培养基所抑制。苍术苷或羧基苍术苷未能阻断藜芦碱刺激的呼吸，但抑制了外源性ADP刺激的呼吸。突触体部分的蛋白质合成被寡霉素、缬氨霉素或2,4-二硝基苯酚所抑制，但不受过量苍术苷的影响。在存在苍术苷的情况下，突触体腺嘌呤核苷酸含量未发现变化，尽管在使用寡霉素、藜芦碱或缬氨霉素时，[ATP]/[ADP]显著降低。这些发现表明，苍术苷不会改变终末内线粒体的能量转导，并且间接表明突触体膜对苍术苷具有不透性。
