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Strathprints serves world leading Open Access research by the University of Strathclyde, including research by the Strathclyde Institute of Pharmacy and Biomedical Sciences (SIPBS), where research centres such as the Industrial Biotechnology Innovation Centre (IBioIC), the Cancer Research UK Formulation Unit, SeaBioTech and the Centre for Biophotonics are based.

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Potassium channel toxins and transmitter release

Harvey, A.L. and Rowan, E.G. and Vatanpour, H. and Fatehi, M. and Castaneda, O. and Karlsson, E. (1994) Potassium channel toxins and transmitter release. Annals of the New York Academy of Sciences, 710. pp. 1-10. ISSN 0077-8923

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Abstract

Much has been learned about the physiological functions of ion channels in neuronal membranes from studies on the effects of naturally occurring neurotoxins. Many toxins have been found to act at Na+, K+, or Ca" channels. In this article, toxins acting on K+ channels to facilitate neurotransmission will be reviewed. Toxins affecting neuronal K + channels have attracted considerable interest recently (for reviews, see references 1-3). They include noxiustoxin from the Mexican scorpion Centruroides no~iusa,p~am in5 and mast cell degranulating peptide6 from the honeybee Apis mellifera, the dendrotoxins from mamba (Dendroaspis) snake^,^ and charybdotoxin from the Old World scorpion Leiurus quinquestriatd (TABLE I). These toxins are highly potent blockers of K+ currents in neurons, but they differ in selectivity for subtypes of K+ channels. For example, apamin blocks certain Caz+-activated K+ channels, whereas the dendrotoxins act on a subset of voltage-dependent K+ channels. Some of the toxins act exclusively on neurons (e.g., dendrotoxins), whereas others affect K+ channels in several different cell types. Actions of toxins on voltagedependent K+ channels and on Ca2+-activated K+ channels and their effects on neuromuscular transmission will be described here.