Nicotinic receptors that bind α-bungarotoxin on neurons raise intracellular free ca2+

Abstract Many populations of vertebrate neurons have a membrane component that binds α-bungarotoxin and cholinergic ligands. Despite the abundance of this component and its similarities to nicotinic receptors, its function has remained controversial. Using a fluorescence assay, we show here that activation of the component elevates the intracellular concentration of free Ca 2+ demonstrating a receptor function for the toxin-binding component. Whole-cell voltage-clamp and intracellular recordings did not detect a significant current resulting from receptor activation, possibly because the currents were small or the receptors rapidly desensitized. The rise in intracellular free Ca 2+ caused by the receptor was prevented by Ca 2+ channel blockers. This suggests a signaling cascade likely to have important regulatory consequences for the neuron.