Abstract
The present experiments tested the uptake, metabolism, and release of choline and two choline analogues, (2-hydroxyethyl)-N-ethyl-N,N-dimethylammonium (monoethylcholine) and N-hydroxyethyl-N-methylpyrrolidinium (pyrrolcholine), by the cat superior cervical ganglion. Both analogues were acetylated in situ, as was choline, and the acetylated derivatives, but not the parent compounds, were released upon subsequent preganglionic nerve stimulation. Like acetylcholine, the release of acetylmonoethylcholine and of acetylpyrrolcholine by nerve impulses required the presence of Ca++. It is concluded that these choline analogues form cholinergic false transmitters. Acetylmonoethylcholine and acetylpyrrolcholine were substrates for acetylcholinesterase. Previous studies showed that acetylmonoethyicholine is less active than acetylcholine as a cholinergic agonist; the present study showed this also for acetylpyrrolcholine. Thus either false transmitter would reduce the safety factor for transmission at cholinergic synapses.
ACKNOWLEDGMENTS We are grateful to Gisèle Johnson and Delia Matriano for technical assistance.
- Copyright © 1976 by Academic Press, Inc.
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