Snelling R, Nicholls D
J Neurochem. 1984 Jun;42(6):1552-7. doi: 10.1111/j.1471-4159.1984.tb12741.x.
The effects of trifluoperazine and 1-[bis(p-chlorophenyl)methyl]-3-[2, 4-dichloro-beta-(2,4- dichlorobenzyloxy )phenethyl]imidazolium chloride ( R2457 ) upon synaptosomal calcium transport, plasma membrane potential, in situ mitochondrial membrane potential, and ATP levels are investigated in order to assess the suitability of these calmodulin antagonists for investigating calmodulin-dependent processes in the nerve terminal. Both agents appear to act selectively at the mitochondrial membrane, causing extensive depolarization at concentrations in excess of 10 microM (trifluoperazine) or 0.5 microM ( R2457 ). The extent of Ca uptake into the synaptosomes is decreased, consistent with the loss of the mitochondrial compartment. There is no inhibition of the efflux of Ca from the synaptosomes. Depolarization-dependent Ca uptake is not prevented by R24571 . Synaptosomal ATP levels decrease to an extent consistent with the collapse of the mitochondrial potential. It is concluded that the uncoupling effect of these agents on the in situ mitochondria prevents their being used to investigate the role of calmodulin in intact synaptosomes.
研究了三氟拉嗪和1-[双（对氯苯基）甲基]-3-[2,4-二氯-β-（2,4-二氯苄氧基）苯乙基]咪唑氯化物（R2457）对突触体钙转运、质膜电位、原位线粒体膜电位和ATP水平的影响，以评估这些钙调蛋白拮抗剂用于研究神经末梢中钙调蛋白依赖性过程的适用性。两种药物似乎都选择性地作用于线粒体膜，在浓度超过10微摩尔/升（三氟拉嗪）或0.5微摩尔/升（R2457）时会引起广泛的去极化。突触体对钙的摄取量减少，这与线粒体区室的丧失一致。突触体中钙的外流没有受到抑制。R24571不能阻止去极化依赖性钙摄取。突触体ATP水平下降的程度与线粒体电位的崩溃一致。得出的结论是，这些药物对原位线粒体的解偶联作用使其无法用于研究钙调蛋白在完整突触体中的作用。
