RT Journal Article
SR Electronic
T1 Modulation of the Neuronal Nicotinic Acetylcholine Receptor-Channel by the Nitromethylene Heterocycle Imidacloprid
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 731
OP 738
VO 285
IS 2
A1 Keiichi Nagata
A1 Jin-Ho Song
A1 Toshio Shono
A1 Toshio Narahashi
YR 1998
UL http://jpet.aspetjournals.org/content/285/2/731.abstract
AB Nitromethylene heterocycle insecticides are known to act on the nicotinic acetylcholine receptor-channel. The effects of the nitromethylene heterocycle, imidacloprid, on the nicotinic acetylcholine receptor-channel of clonal rat phaeochromocytoma (PC12) cells were studied using whole-cell and single-channel patch clamp methods. Imidacloprid suppressed carbachol-induced whole-cell currents in a dose-dependent manner, and this compound itself generated small currents. Multiple conductance states of single-channel currents were also evoked by imidacloprid at the nicotinic acetylcholine receptor-channels. The most frequently generated single-channel currents showed two conductance states, 25.4 and 9.8 pS, which were identical to the conductance states of acetylcholine-generated currents. The mean open time and burst duration of the main conductance currents induced by imidacloprid were shorter than those induced by acetylcholine. Co-application of imidacloprid and acetylcholine caused some interactions at the two conductance states. Mean open time and mean burst duration of the main conductance state currents evoked by acetylcholine were decreased by the co-application of imidacloprid as compared with those induced by acetylcholine alone. In conclusion, imidacloprid has both multiple agonist and antagonist effects on the neuronal nicotinic acetylcholine receptor-channels. The American Society for Pharmacology and Experimental Therapeutics