Schweitzer E S, Blaustein M P
Biochim Biophys Acta. 1980 Aug 14;600(3):912-21. doi: 10.1016/0005-2736(80)90493-9.
The particulate fraction from osmotically shocked synaptosomes ('synaptosomal membrances') sequesters Ca when incubated with ATP]containing solutions. This net accumulation of Ca can reduce the free [Ca2+] of the bathing medium to sub-micromolar levels (measured with arsenazo III). Two distinct types of Ca sequestration site are responsible for the Ca2+ buffering. One site, presumed to be smooth endoplasmic reticulum, operates at low [Ca2+] (less than 1 microM), and has a relatively small capacity. Ca sequestration at this site is prevented by the Ca2+ ionophore, A-23187, but not by mitochondrial poisons. The secone (mitochondrial) site, in contrast, is blocked by the mitochondrial uncoupler carbonyl cyanide p-trifluoromethoxyphenylhydrazone, and oligomycin. Since the intraterminal organelles can buffer [Ca2+] to about 0.3-0.5 microM, this may be an upper limit to the normal resting level of [Ca2+]i in nerve terminals. In the steady state, total cell Ca and [Ca2+]i will be governed principally be Ca transport mechanisms in the plasmalemma; the intracellular organelle transport systems then operate in equilibrium with this [Ca2+]. During activity, however, Ca rapidly enters the terminals and [Ca2+]i rises. The intracellular buffering mechanisms then come into play and help to return [Ca2+]i toward the resting level; the non-mitochondrial Ca sequestration mechanism probably plays the major role in this Ca buffering.
经渗透压休克处理的突触体（“突触体膜”）的微粒部分在与含ATP的溶液一起孵育时会螯合钙。钙的这种净积累可将浴液介质中的游离[Ca2+]降低至亚微摩尔水平（用偶氮胂III测量）。两种不同类型的钙螯合位点负责Ca2+缓冲。一个位点，推测为光滑内质网，在低[Ca2+]（小于1 microM）下起作用，且容量相对较小。该位点的钙螯合可被Ca2+离子载体A-23187阻止，但不受线粒体毒物影响。相比之下，第二个（线粒体）位点被线粒体解偶联剂羰基氰化物对三氟甲氧基苯腙和寡霉素阻断。由于终末内细胞器可将[Ca2+]缓冲至约0.3 - 0.5 microM，这可能是神经末梢中[Ca2+]i正常静息水平的上限。在稳态下，细胞总钙和[Ca2+]i将主要由质膜中的钙转运机制控制；细胞内细胞器转运系统随后与这种[Ca2+]处于平衡状态。然而，在活动期间，钙迅速进入末梢，[Ca2+]i升高。细胞内缓冲机制随后发挥作用，帮助[Ca2+]i恢复到静息水平；非线粒体钙螯合机制可能在这种钙缓冲中起主要作用。
