Vickers G R, Dowdall M J
Exp Brain Res. 1976 Jun 30;25(4):429-45. doi: 10.1007/BF00241732.
Energy dependent 45Ca2+ uptake in the synaptosomal preparation from guinea pig cortex has been investigated. 45Ca2+ uptake was stimulated by ATP, the absolute value of uptake being dependent on the extent of synaptosomal disruption caused by osmotic shock. A quantitative comparison of microsomal and mitochondrial ATP-dependent 45Ca2+ uptake showed that only mitochondria had a large enough capacity to account for the Ca uptake levels observed in the synaptosomal preparation. ATP-stimulated 45Ca2+ uptake in mitochondria, 'intact' and 'shocked' synaptosomes was inhibited by atractyloside, DNP, oligomycin and ruthenium red but unaffected by antimycin A and rotenone. This was interpreted as evidence that mitochondria were responsible for ATP-dependent synaptosomal Ca2+ uptake, the increase in uptake seen on osmotic lysis being due to the deocclusion of intraterminal mitochondria. Synaptosomal and mitochondrial 45Ca2+ uptake was also stimulated by the mitochondrial respiratory substrate glutamate; this uptake was sensitive to antimycin A, DNP, rotenone and ruthenium red but insensitive to atractyloside or oligomycin thus indicating it was of mitochondrial origin. No change in glutamate-dependent 45Ca2+ uptake was seen on osmotic lysis of the synaptosomes as the expected increase due to the release of occluded mitochondria was counterbalanced by the damaging effect of hypo-osmotic shock on the glutamate-stimulated 45Ca2+ uptake process.
对豚鼠皮层突触体制剂中能量依赖性的45Ca2+摄取进行了研究。ATP刺激了45Ca2+的摄取，摄取的绝对值取决于渗透压休克引起的突触体破坏程度。微粒体和线粒体ATP依赖性45Ca2+摄取的定量比较表明，只有线粒体具有足够大的容量来解释突触体制剂中观察到的钙摄取水平。线粒体、“完整”和“休克”突触体中ATP刺激的45Ca2+摄取受到苍术苷、二硝基苯酚、寡霉素和钌红的抑制，但不受抗霉素A和鱼藤酮的影响。这被解释为线粒体负责ATP依赖性突触体Ca2+摄取的证据，渗透压裂解时摄取增加是由于终末内线粒体的去封闭。突触体和线粒体的45Ca2+摄取也受到线粒体呼吸底物谷氨酸的刺激；这种摄取对抗霉素A、二硝基苯酚、鱼藤酮和钌红敏感，但对苍术苷或寡霉素不敏感，因此表明它起源于线粒体。突触体渗透压裂解时，谷氨酸依赖性45Ca2+摄取没有变化，因为由于封闭线粒体释放而预期的增加被低渗休克对谷氨酸刺激的45Ca2+摄取过程的破坏作用所抵消。
