Bielarczyk H, Szutowicz A
Department of Clinical Biochemistry, Medical Academy, Gdańsk, Poland.
Biochem J. 1989 Aug 15;262(1):377-80. doi: 10.1042/bj2620377.
Isolated synaptosomes maintained a relatively stable level of acetyl-CoA during their incubation in the presence of 30 mM-KCl. Addition of Ca2+ resulted in inhibition of pyruvate oxidation and slight activation of acetylcholine synthesis. The cation decreased acetyl-CoA in intrasynaptosomal mitochondria, but did not alter its content in synaptoplasm. Verapamil did not affect pyruvate oxidation, but decreased acetyl-CoA in synaptoplasm and inhibited acetylcholine synthesis in synaptosomes. It indicates that Ca2+ might regulate acetylcholine synthesis through changes in the direct transfer of acetyl-CoA from mitochondria to synaptoplasm.
在含有30 mM - KCl的条件下孵育时,分离的突触体维持着相对稳定水平的乙酰辅酶A。添加Ca2+会导致丙酮酸氧化受到抑制,乙酰胆碱合成略有激活。该阳离子降低了突触体内线粒体中的乙酰辅酶A,但并未改变其在突触质中的含量。维拉帕米不影响丙酮酸氧化,但降低了突触质中的乙酰辅酶A,并抑制了突触体中的乙酰胆碱合成。这表明Ca2+可能通过改变乙酰辅酶A从线粒体到突触质的直接转运来调节乙酰胆碱的合成。