Cellular and Molecular Neurobiology

, Volume 25, Issue 3, pp 513–552

Nicotinic Agonists, Antagonists, and Modulators From Natural Sources

Authors

    • Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney DiseasesNational Institutes of Health, DHHS
    • National Institutes of Health
Article

DOI: 10.1007/s10571-005-3968-4

Cite this article as:
Daly, J.W. Cell Mol Neurobiol (2005) 25: 513. doi:10.1007/s10571-005-3968-4

Abstract

1. Acetylcholine receptors were initially defined as nicotinic or muscarinic, based on selective activation by two natural products, nicotine and muscarine. Several further nicotinic agonists have been discovered from natural sources, including cytisine, anatoxin, ferruginine, anabaseine, epibatidine, and epiquinamide. These have provided lead structures for the design of a wide range of synthetic agents.

2. Natural sources have also provided competitive nicotinic antagonists, such as the Erythrina alkaloids, the tubocurarines, and methyllycaconitine. Noncompetitive antagonists, such as the histrionicotoxins, various izidines, decahydroquinolines, spiropyrrolizidine oximes, pseudophrynamines, ibogaine, strychnine, cocaine, and sparteine have come from natural sources. Finally, galanthamine, codeine, and ivermectin represent positive modulators of nicotinic function, derived from natural sources.

3. Clearly, research on acetylcholine receptors and functions has been dependent on key natural products and the synthetic agents that they inspired.

Key Words

anatoxincocainecytisinedihydro-beta-erythroidineepibatidineepiquinamidegalanthaminehistrionicotoxinibogainemethyllycaconitinemuscarinenicotinenoncompetitive antagoniststubocurarine
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Copyright information

© Springer Science + Business Media, Inc. 2005