Acetyltriethylcholine: a cholinergic false transmitter in cat superior cervical ganglion and rat cerebral cortex.

Abstract

Abstract—The accumulation and metabolism of [14C]triethylcholine by cat superior cervical ganglia [rested or stimulated (20 Hz)] and by rat cerebral cortex minces was measured. In ganglia, preganglionic nerve stimulation increased the accumulation (2.4 fold) and the acetylation (5.7 fold) of triethylcholine; however the depletion of the ganglion's acetylcholine content was 9.5 times greater than the amount of acetyltriethylcholine synthesized. In the presence of eserine, neither stimulated nor rested ganglia synthesized any extra (surplus) acetyltriethylcholine. It is concluded that the rate‐limiting step in acetyltriethylcholine synthesis is the acetylation of triethylcholine by choline acetyltransferase. Subsequent preganglionic nerve stimulation of ganglia, which had been stimulated during the exposure to [14C]‐triethylcholine, caused the increased release of only acetyltriethylcholine; the release was frequency‐dependent, required the presence of Ca2+, and was blocked by increasing the ratio of Mg2+/Ca2+ in the perfusion fluid. All of the acetyltriethylcholine which had been accumulated was available for release. Rat cerebral cortex also accumulated triethylcholine and acetylated about 3% of the accumulated choline analogue. Subsequent stimulation by high K+ (46 mM)‐atropine (3 μM) caused the increased release of acetyltriethylcholine from the cortex and this release required the presence of Ca2+. Triethylcholine can therefore form a cholinergic false transmitter in the cat superior cervical ganglion and the rat cerebral cortex.