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Potassium Channel Toxins and Transmitter Release
Author(s) -
HARVEY A. L.,
ROWAN E. G.,
VATANPOUR H.,
FATEHI M.,
CASTANEDA O.,
KARLSSON E.
Publication year - 1994
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1994.tb26609.x
Subject(s) - rowan , medicine , library science , physiology , biology , computer science , ecology
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