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Open Access research with a European policy impact...

The Strathprints institutional repository is a digital archive of University of Strathclyde's Open Access research outputs. Strathprints provides access to thousands of Open Access research papers by Strathclyde researchers, including by researchers from the European Policies Research Centre (EPRC).

EPRC is a leading institute in Europe for comparative research on public policy, with a particular focus on regional development policies. Spanning 30 European countries, EPRC research programmes have a strong emphasis on applied research and knowledge exchange, including the provision of policy advice to EU institutions and national and sub-national government authorities throughout Europe.

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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.