Heinonen E, Akerman K E, Kaila K
Neurosci Lett. 1984 Aug 24;49(1-2):33-7. doi: 10.1016/0304-3940(84)90132-0.
Intracellular calcium transients in synaptosomes, isolated from the guinea pig brain, were measured using entrapped metallochromic indicator arsenazo III. Addition of 1 microM carbonyl cyanide p-trifluoromethoxyphenyl hydrazone (FCCP) increased rapidly the absorbance of the entrapped arsenazo III, indicating an increase in the cytosolic free calcium. The FCCP-induced increase in cytoplasmic free Ca2+ was not blocked by 200 microM verapamil, while the increment in calcium caused by 40 microM veratridine was verapamil-sensitive. The absorbance changes induced by FCCP were not significantly increased when the extracellular potassium concentration was elevated from 5.4 to 50 mM. These data indicate that in nerve endings of mammalian brain, cytoplasmic free calcium, which is essential for the release of transmitter, is increased on depolarization of major intracellular calcium buffers, mitochondria.
使用包埋的金属铬指示剂偶氮胂III测量从豚鼠脑分离的突触体中的细胞内钙瞬变。添加1微摩尔羰基氰化物对三氟甲氧基苯腙（FCCP）会迅速增加包埋的偶氮胂III的吸光度，表明胞质游离钙增加。FCCP诱导的细胞质游离Ca2+增加未被200微摩尔维拉帕米阻断，而40微摩尔藜芦定引起的钙增加对维拉帕米敏感。当细胞外钾浓度从5.4毫摩尔升高到50毫摩尔时，FCCP诱导的吸光度变化没有显著增加。这些数据表明，在哺乳动物脑的神经末梢中，对于递质释放至关重要的胞质游离钙在主要细胞内钙缓冲剂线粒体去极化时会增加。
