MolPharm xPharm- The Comprehensive Pharmacology Reference

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by COLLIER, B.
Right arrow Articles by MITTAG, T. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by COLLIER, B.
Right arrow Articles by MITTAG, T. W.

Molecular Pharmacology, Vol 12, 340-344, Copyright © 1976 by the American Society for Pharmacology and Experimental Therapeutics

The Release of Acetylated Choline Analogues by a Sympathetic Ganglion

B. COLLIER 1, L. A. BARKER 2, and T. W. MITTAG 2

1 Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec, Canada H3G1Y6
2 Department of Pharmacology, Mount Sinai School of Medicine of the City University of New York, New York 10029

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.

Note:
ACKNOWLEDGMENTS We are grateful to Gisèle Johnson and Delia Matriano for technical assistance.

Submitted on September 5, 1975




This article has been cited by other articles:


Home page
 ScienceHome page
D. Jenden, R. Jope, and M. Weiler
Regulation of acetylcholine synthesis: does cytoplasmic acetylcholine control high affinity choline uptake?
Science, November 5, 1976; 194(4265): 635 - 637.
[Abstract] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
Molecular Interventions Drug Metabolism and Disposition

Copyright © 1976 by the American Society for Pharmacology and Experimental Therapeutics