Fossier P, Diebler M F, Mothet J P, Israel M, Tauc L, Baux G
Laboratoire de Neurobiologie Cellulaire et Moléculaire, C.N.R.S., Gif sur Yvette, France.
Neuroscience. 1998 Jul;85(1):85-91. doi: 10.1016/s0306-4522(97)00591-5.
2,5-Diterbutyl-1,4-benzohydroquinone, a specific blocker of Ca2+-ATPase pumps, increased acetylcholine release from an identified synapse of Aplysia, as well as from Torpedo and mouse caudate nucleus synaptosomes. Because 2,5-diterbutyl-1,4-benzohydroquinone does not change the presynaptic Ca2+ influx, the enhancement of acetylcholine release could be due to an accumulation of Ca2+ in the terminal. This possibility was further checked by studying the effects of 2,5-diterbutyl-1,4-benzohydroquinone on twin pulse facilitation, classically attributed to residual Ca2+. While preventing the fast sequestration of Ca2+ by presynaptic organelles, 2,5-diterbutyl-1,4-benzohydroquinone magnified both twin pulse facilitation observed under low extracellular Ca2+ concentration and twin pulse dysfacilitation observed under high extracellular Ca2+ concentration. Thus, it is concluded that 2,5-diterbutyl-1,4-benzohydroquinone, by preventing Ca2+ buffering near transmitter release sites, modulates acetylcholine release. As 2,5-diterbutyl-1,4-benzohydroquinone was also shown to decrease by 50% the uptake of 45Ca2+ by isolated synaptic vesicles, we propose that synaptic vesicles can control the presynaptic Ca2+ concentration triggering the release of neurotransmitter.
2,5 - 二叔丁基 - 1,4 - 苯二酚，一种Ca2 + - ATP酶泵的特异性阻滞剂，可增加从海兔的一个已确定突触以及电鳐和小鼠尾状核突触小体中乙酰胆碱的释放。由于2,5 - 二叔丁基 - 1,4 - 苯二酚不会改变突触前Ca2 + 的内流，乙酰胆碱释放的增强可能是由于终末中Ca2 + 的积累。通过研究2,5 - 二叔丁基 - 1,4 - 苯二酚对双脉冲易化（传统上归因于残余Ca2 + ）的影响，进一步检验了这种可能性。在阻止突触前细胞器对Ca2 + 的快速隔离的同时，2,5 - 二叔丁基 - 1,4 - 苯二酚放大了在低细胞外Ca2 + 浓度下观察到的双脉冲易化以及在高细胞外Ca2 + 浓度下观察到的双脉冲去易化。因此，得出结论，2,5 - 二叔丁基 - 1,4 - 苯二酚通过阻止递质释放位点附近的Ca2 + 缓冲来调节乙酰胆碱的释放。由于2,5 - 二叔丁基 - 1,4 - 苯二酚还被证明可使分离的突触小泡对45Ca2 + 的摄取减少50%，我们提出突触小泡可以控制触发神经递质释放的突触前Ca2 + 浓度。
