Ks. Hsu et al., BLOCKADE BY 2,2',2''-TRIPYRIDINE OF THE NICOTINIC ACETYLCHOLINE-RECEPTOR CHANNELS IN EMBRYONIC XENOPUS MUSCLE-CELLS, British Journal of Pharmacology, 110(1), 1993, pp. 163-168
1 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',2''-Tripyridine depressed the amplitude of
iontophoretic ACh-induced current at a low frequency of 0.7 Hz stimul
ation and it not only decreased the initial responses but also enhance
d the run-down of ACh-induced current at higher frequency stimulation
of 7 Hz and 30 Hz. 3 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 channel
s. 4 These results suggest that the blocking actions of 2,2',2''-tripy
ridine on ACh receptor channels in the skeletal muscle may contribute
to the depression of the nerve-evoked contraction of the mouse diaphra
gm as reported previously.