Whole-cell recording techniques were used to examine acetylcholine-induced nicotinic currents in isolated bovinei chromaffin cells. The effects on these currents of κ-bungarotoxin, a snake venon κ-neurotoxin, were tested. Exposure of cells to κ-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 κ-bungarotoxin. Secondly, voltage-clamp measurements indicated that the degree of blockade produced by κ-bungarotoxin was independent of cell membrane potential. Unlike (+)-tubocurarine, κ-bungarotoxin had no direct agonist effects on nicotinic receptors. It is concluded from the present functional studies and from previously reported binding studies that κ-bungarotoxin blocks nicotinic responses in bovine chromaffin cells by binding to regions overlying acetylcholine sites on nicotinic receptors.
- Bovine adrenomedullary chromaffin cell
- Nicotinic receptor