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Potassium Channel Toxins

  • Chapter
Selective Neurotoxicity

Part of the book series: Springer Study Edition ((SSE,volume 102))

Abstract

The past decade has seen rapid progress in our knowledge about K channels and their pharmacology. Various types have been discovered: voltage-gated (separated into delayed rectifier, inward rectifier, transiently activating channels); Ca-activated [subdivided into high conductance (150-250pS) and low conductance (10-14pS) channels]; Na-activated; ATP-sensitive; M channels (inhibited by acetylcholine acting through muscarinic receptors); and S channels (inhibited by a cAMP-dependent protein kinase through serotonin receptors). Twelve years ago, the first report that an animal toxin (the bee venom toxin apamin) blocks a certain type of K channel (the Caactivated K channel of hepatocytes) appeared (Banks et al. 1979). Three years later, a fraction of the venom of the scorpion Centruroides noxius was found to depress the permeability of voltage-dependent K channels (but not of Na channels ) (Carbone et al. 1982). A further milestone in the toxinology of K channels was the discovery that dendrotoxin, a potent convulsant purified from the venom of mamba snakes (Harvey and Karlsson 1980), selectively blocks a transient K conductance in hippocampal neurons (Dolly et al. 1984). Great interest was also attracted by charybdotoxin, a fraction of the venom of the scorpion Leiurus quinquestriatus; it has a high affinity for Ca-activated K channels of high conductance (Miller et al. 1985) but is also a potent blocker of voltage-sensitive K channels.

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Note Added in Proof:Several further papers on potassium channel toxins have appeared:Apamin

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Meves, H. (1994). Potassium Channel Toxins. In: Herken, H., Hucho, F. (eds) Selective Neurotoxicity. Springer Study Edition, vol 102. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-85117-9_21

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