IMR32 cells express two classes of surface nicotinic receptors: those labelled with high affinity by [125I]neuronal toxin, and those labelled by [125Iα-bungarotoxin. Whole-cell patch-clamp recordings indicate that both classes of receptor are able to elicit inward currents that are totally blocked by d-tubocurarine but only partially blocked by α-bungarotoxin. In IMR32 cells, nicotine induces an increase in the intracellular level of free Ca2+. This increase, which is also completely blocked by d-tubocurarine and only partially blocked by α-bungarotoxin and Cd2+, is due to extracellular calcium influx through both the nicotinic receptors and the voltage-activated Ca2+ channels. By using subunit-specific polyclonal antibodies, we have demonstrated that the α-bungarotoxin receptors contain the α7 subunit, but none of the other subunits whose transcripts are present in IMR32 cells. The pharmacological profile of these human α7-containing α-bungarotoxin receptors is similar to that observed in the native chick α7 receptor, but there are also some species-specific differences.