Snelling R, Nicholls D
Biochem J. 1985 Feb 15;226(1):225-31. doi: 10.1042/bj2260225.
Ca2+ efflux from intact synaptosomes is investigated. Net efflux can be induced by returning synaptosomes from media with elevated Ca2+ or high pH to a normal medium. Net Ca2+ efflux is accelerated when the Na+ electrochemical potential gradient is collapsed by veratridine plus ouabain. Under steady-state conditions at 30 degrees C, Ca2+ cycles across the plasma membrane at 0.38 nmol . min-1 . mg-1 of protein. Exchange is increased by 145% by veratridine plus ouabain, both influx and efflux being increased. Increased influx is probably due to activation of voltage-dependent Ca2+ channels, since it is abolished by verapamil. The results indicate that, at least under conditions of low Na+ electrochemical gradient, some pathway other than a Na+/Ca2+ exchange must operate in the plasma membrane to expel Ca2+.
对完整突触体的Ca2+外流进行了研究。当将突触体从Ca2+浓度升高或pH值较高的培养基转移至正常培养基时,可诱导净外流。当用藜芦碱加哇巴因使Na+电化学势梯度消失时,净Ca2+外流加速。在30℃的稳态条件下,Ca2+以0.38 nmol·min-1·mg-1蛋白质的速率跨质膜循环。藜芦碱加哇巴因可使交换增加145%,流入和流出均增加。流入增加可能是由于电压依赖性Ca2+通道的激活,因为维拉帕米可消除这种增加。结果表明,至少在低Na+电化学梯度条件下,质膜中必须存在除Na+/Ca2+交换以外的其他途径来排出Ca2+。