Toll L, Gundersen C B, Howard B D
Brain Res. 1977 Nov 4;136(1):59-66. doi: 10.1016/0006-8993(77)90131-7.
Several inhibitors of energy metabolism decreased the ATP-stimulated uptake of catecholamines by isolated synaptic vesicles from rat brain and by chromaffin granules from bovine adrenal medulla. Catecholamine uptake was inhibited by dinitrophenol, S-13 and oleic acid, which are known to block active transport by dissipating trans-membrane proton gradients. Thus a proton gradient appears to be involved in catecholamine transport. Both catecholamine uptake and vesicle-associated Ca2+/Mg2+-ATPase were inhibited by dicyclohexylcarbodiimide and tributyltin, which had previously been shown to inhibit the Ca2+/Mg2+-ATPase of mitochondria. However, mitochondrial ATPase was not involved in catecholamine uptake as oligomycin and aurovertin, more specific inhibitors of mitochondrial ATPase, did not affect catecholamine uptake. It is suggested that ATP stimulates catecholamine uptake by serving as a substrate for the ATPase. Activity of this enzyme causes translocation of protons across the vesicle membrane establishing a trans-membrane proton gradient. The proton gradient drives the transport of catecholamines.
几种能量代谢抑制剂降低了从大鼠脑分离出的突触小泡以及从牛肾上腺髓质分离出的嗜铬颗粒对ATP刺激的儿茶酚胺摄取。二硝基苯酚、S - 13和油酸抑制了儿茶酚胺摄取，已知它们通过消耗跨膜质子梯度来阻断主动转运。因此，质子梯度似乎参与了儿茶酚胺转运。二环己基碳二亚胺和三丁基锡抑制了儿茶酚胺摄取以及与小泡相关的Ca2+/Mg2+-ATP酶，先前已表明它们能抑制线粒体的Ca2+/Mg2+-ATP酶。然而，线粒体ATP酶并不参与儿茶酚胺摄取，因为寡霉素和金雀花碱（线粒体ATP酶更特异的抑制剂）并不影响儿茶酚胺摄取。有人提出，ATP通过作为ATP酶的底物来刺激儿茶酚胺摄取。该酶的活性导致质子跨小泡膜转运，建立跨膜质子梯度。质子梯度驱动儿茶酚胺的转运。
