Imidacloprid is increasingly used worldwide as an insecticide. It is an ago
nist at nicotinic acetylcholine receptors (nAChRs) and shows selective toxi
city for insects over vertebrates. Recent studies using binding assays, mol
ecular biology and electrophysiology suggest that both alpha- and non-alpha
-subunits of nAChRs contribute to interactions of these receptors with imi
dacloprid. Electrostatic interactions of the nitroimine group and bridgehea
d nitrogen in imidacloprid with particular nAChR amino acid residues are li
kely to have key roles in determining the selective toxicity of imidaclopri
d. Chemical calculation of atomic charges of the insecticide molecule and a
site-directed mutagenesis study support this hypothesis.