Actions of imidacloprid and a related nitromethylene on cholinergic receptors of an identified insect motor neurone

Abstract Nitromethylenes and their analogues are a novel class of insecticidally active molecules of commercial importance. Here we describe the actions of a novel nitroguanidine analogue, l‐(6‐chloro‐3‐pyridylmethyl)‐N‐nitroimidazolidin‐2‐ylideneamine (imidacloprid; NTN 33893) and a nitromethylene, l‐(3‐pyridylmethyl)‐2‐nitromethylene‐imidazolidine (PMNI) on the cockroach fast coxal depressor motor neurone Df and their effectiveness in displacing [125I]α‐bungarotoxin binding to cockroach nerve cord preparations. When tested on the cell body of this identified neurone both imidacloprid and PMNI induce slow depolarizations, which are sensitive to nicotinic receptor antagonists, such as dihydro‐β‐erythroidine (1.0 × 10−5 M) and mecamylamine (1.0 × 10−4 M). Lower concentrations of imidacloprid (1.0 × 10−8 −1.0 × 10−6 M) and PMNI (1.0 × 10−8 M) show no antagonist action on nicotine‐induced depolarization. At concentrations in the range 1.0 × 10−7 −5.0 × 10−7 M, PMNI partially and reversibly blocks nicotine‐induced depolarization. Both compounds are more effective displacers of specific [125I]α‐bungarotoxin binding than nicotine, with imidacloprid (IC50 = 2.0 × 10−7 M) about tenfold more potent than PMNI (IC50 = 1.3 × 10−6 M).