Tomaszewicz M, Bielarczyk H, Jankowska A, Szutowicz A
Department of Clinical Biochemistry, School of Medicine, Gdańsk.
Folia Neuropathol. 1997;35(4):244-6.
beta-hydroxybutyrate increased concentration of acetyl-CoA in mitochondria of resting and in cytoplasm of Ca-activated rat brain synaptosomes. Adequate rise of Ca-evoked acetylcholine release was also observed. The activation was abolished by verapamil. It indicates that beta-hydroxybutyrate-derived acetyl-CoA is transported from mitochondria to synaptoplasm by direct Ca-dependent transport mechanism. Presented data evidence that level of synaptoplasmic acetyl-CoA plays an important role in the regulation of cholinergic activity in the brain.
β-羟基丁酸增加了静息大鼠脑突触体线粒体以及钙激活的大鼠脑突触体细胞质中乙酰辅酶A的浓度。还观察到钙诱发的乙酰胆碱释放有适当增加。维拉帕米可消除这种激活作用。这表明β-羟基丁酸衍生的乙酰辅酶A通过直接的钙依赖转运机制从线粒体转运至突触质。现有数据证明，突触质中乙酰辅酶A的水平在大脑胆碱能活性的调节中起重要作用。
