Nooney J M, Lambert J J, Chiappinelli V A
Department of Pharmacology and Clinical Pharmacology, Ninewells Hospital, University of Dundee, U.K.
Brain Res. 1992 Feb 21;573(1):77-82. doi: 10.1016/0006-8993(92)90115-p.
Whole-cell recording techniques were used to examine acetylcholine-induced nicotinic currents in isolated bovine chromaffin cells. The effects on these currents of kappa-bungarotoxin, a snake venom kappa-neurotoxin, were tested. Exposure of cells to kappa-bungarotoxin (600 nM for 40 min) produced a prolonged blockade of nicotinic currents. The mechanism of this blockade was examined in several ways. Firstly, the pre-exposure of cells to trimetaphan, a competitive nicotinic antagonist, protected against the action of subsequent additions of kappa-bungarotoxin. Secondly, voltage-clamp measurements indicated that the degree of blockade produced by kappa-bungarotoxin was independent of cell membrane potential. Unlike (+)-tubocurarine, kappa-bungarotoxin had no direct agonist effects on nicotinic receptors. It is concluded from the present functional studies and from previously reported binding studies that kappa-bungarotoxin blocks nicotinic responses in bovine chromaffin cells by binding to regions overlying acetylcholine sites on nicotinic receptors.