Tuchek S, Dolezhal V, Richny Ia
Neirofiziologiia. 1984;16(5):603-11.
Data on the acetylcholine (ACh) synthesis in nerve cells with special attention to its control are summarized in the paper. At rest or during moderate synaptic activity, the concentration of ACh in the compartment of its synthesis probably corresponds to the equilibrium between the substrates and products in the reaction catalysed by choline acetyltransferase. The release of ACh is followed by a transfer of ACh from the compartment of its synthesis to the compartment of release, and, automatically, by the synthesis of new ACh until a new equilibrium is reached in the compartment of synthesis. In addition, synaptic activity and the release of ACh support the synthesis of new ACh in the following ways: choline carriers are disinhibited by lowering the concentration of ACh in the nerve endings, and the transport of choline from the extracellular fluid to the cell interior according to its electro-chemical gradient is thus facilitated; the concentration of choline in the extracellular fluid is increased in the vicinity of the nerve endings as a consequence of the hydrolysis of the released ACh; postactivation hyperpolarization of the nerve endings brings about an increase of the choline transport and concentration in the nerve endings; presumably, the stimulation of muscarinic receptors brings about a further increase in the choline concentration in the vicinity of the nerve endings by the phosphatidylcholine hydrolysis intensification in postsynaptic cells; the decrease in the concentration of acetyl-CoA (as a consequence of the resynthesis of ACh) increases the activity of pyruvate dehydrogenase and the production of acetyl-CoA; conceivably, the increase in the concentration of Ca2+ ions in the nerve endings assists direct passage of acetyl-CoA from the mitochondria to the cytosol of the nerve endings, where the synthesis of ACh occurs.(ABSTRACT TRUNCATED AT 250 WORDS)
本文总结了神经细胞中乙酰胆碱(ACh)合成的数据,特别关注其调控机制。在静息状态或适度突触活动期间,ACh合成区室中的ACh浓度可能与胆碱乙酰转移酶催化反应中底物和产物之间的平衡相对应。ACh释放后,ACh从合成区室转移至释放区室,同时自动引发新ACh的合成,直至合成区室达到新的平衡。此外,突触活动和ACh释放通过以下方式支持新ACh的合成:降低神经末梢中ACh的浓度可解除胆碱载体的抑制作用,从而促进胆碱根据其电化学梯度从细胞外液转运至细胞内;释放的ACh水解导致神经末梢附近细胞外液中胆碱浓度升高;神经末梢激活后超极化会使神经末梢中胆碱转运和浓度增加;推测毒蕈碱受体的刺激会通过增强突触后细胞中磷脂酰胆碱的水解,使神经末梢附近的胆碱浓度进一步升高;ACh重新合成导致乙酰辅酶A浓度降低,会增加丙酮酸脱氢酶的活性及乙酰辅酶A的生成;可以想象,神经末梢中Ca2+离子浓度的增加有助于乙酰辅酶A从线粒体直接进入ACh合成所在的神经末梢胞质溶胶。(摘要截选至250词)