Effects of Extracellular Choline Concentration and K+Depolarization on Choline Kinase and Choline Acetyltransferase Activities in Superior Cervical Sympathetic Ganglia Excised from Rats

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Abstract
The activities of choline kinase (CK) and choline acetyltransferase (ChAT) were examined in vitro in superior cervical sympathetic ganglia (SCG) excised from rats following aerobic incubation for 1 h in a medium containing various choline concentrations, with and without application of a high KCl level (70 mM). Ganglionic CK activity was strongly inhibited (by .apprx. 75%) at low extracellular choline concentrations (1-5 .mu.M) but rose as the choline concentration was raised to 10-50 .mu.M in the incubation medium, then fell and rose again with further increases in choline concentration. A similar but moderate accelerative effect on ganglionic CK activity was also observed after addition of acetylcholine (ACh; 1 mM) without eserine. Whereas specific CK activity did not change significantly in axotomized SCG, in which the ratio of glial cells to neurons is greatly increased for a week after the operation, it was remarkably increased after denervation, in which the preganglionic cholinergic nerve terminals had degenerated. When either a high KCl level or hemicholinium-3 (HC-3; 50 .mu.M) was added to the medium in the presence or absence of choline, ganglionic CK activity was markedly inhibited. On the other hand, ChAT activity in the SCG remained at a significantly high level during incubation with low choline concentrations (1-10 .mu.M), but the enhanced enzyme activity became inhibited as the extracellular choline concentration was raised to 50-100 .mu.M in the medium. Addition of HC-3 to the medium did not alter ganglionic ChAT activity at low choline concentrations. However, application of quinacrine (10 .mu.M) considerably reduced ganglionic CK activity and also suppressed ChAT activity induced by high KCl levels. These reciprocal fluctuating changes of ganglionic CK and ChAT activities as a function of extracellular choline concentration in the incubation medium strongly suggest that cytoplasmic CK might contribute to modulating the supply of choline, after uptake from the extracellular fluid, either for storage in membranous phosphatidylcholine (lecithin) or for synthesis of the neurotransmitter ACh by ChAT in cholinergic nerve terminals.