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Ciguatoxins: Cyclic Polyether Modulators of Voltage-gated Iion Channel Function
Neurotoxin Research Group, Department of Health Sciences, University of Technology, Sydney, PO Box 123, Broadway NSW 2007, Australia
Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD 4072, Australia
* Author to whom correspondence should be addressed.
Received: 21 December 2005; Accepted: 9 March 2006 / Published: 6 April 2006
Abstract: Ciguatoxins are cyclic polyether toxins, derived from marine dinoflagellates, which are responsible for the symptoms of ciguatera poisoning. Ingestion of tropical and subtropical fin fish contaminated by ciguatoxins results in an illness characterised by neurological, cardiovascular and gastrointestinal disorders. The pharmacology of ciguatoxins is characterised by their ability to cause persistent activation of voltage-gated sodium channels, to increase neuronal excitability and neurotransmitter release, to impair synaptic vesicle recycling, and to cause cell swelling. It is these effects, in combination with an action to block voltage-gated potassium channels at high doses, which are believed to underlie the complex of symptoms associated with ciguatera. This review examines the sources, structures and pharmacology of ciguatoxins. In particular, attention is placed on their cellular modes of actions to modulate voltage-gated ion channels and other Na+-dependent mechanisms in numerous cell types and to current approaches for detection and treatment of ciguatera.
Keywords: ciguatoxin; dinoflagellate; Gambierdiscus toxicus; voltage-gated sodium channel; voltage-channel potassium channel
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MDPI and ACS Style
Nicholson, G.M.; Lewis, R.J. Ciguatoxins: Cyclic Polyether Modulators of Voltage-gated Iion Channel Function. Mar. Drugs 2006, 4, 82-118.
Nicholson GM, Lewis RJ. Ciguatoxins: Cyclic Polyether Modulators of Voltage-gated Iion Channel Function. Marine Drugs. 2006; 4(3):82-118.
Nicholson, Graham M.; Lewis, Richard J. 2006. "Ciguatoxins: Cyclic Polyether Modulators of Voltage-gated Iion Channel Function." Mar. Drugs 4, no. 3: 82-118.