Blockade by 2,2′,2″‐tripyridine of the nicotinic acetylcholine receptor channels in embryonic Xenopus muscle cells

The effects of 2,2′,2″‐tripyridine on the nicotinic acetylcholine (ACh) receptor channels were studied in the cultured myocytes of 1‐day‐old Xenopus embryos. 2,2′,2″‐Tripyridine depressed the amplitude of iontophoretic ACh‐induced current at a low frequency of 0.7 Hz stimulation and it not only decreased the initial responses but also enhanced the run‐down of ACh‐induced current at higher frequency stimulation of 7 Hz and 30 Hz. Single ACh channel recordings showed that 2,2′,2″‐tripyridine decreased the channel conductance, the opening frequency and mean open time of both types of low‐ and high‐conductance channels. These results suggest that the blocking actions of 2,2′,2″‐tripyridine on ACh receptor channels in the skeletal muscle may contribute to the depression of the nerve‐evoked contraction of the mouse diaphragm as reported previously. 1993 British Pharmacological Society