Abstract

To elucidate the mechanism of selective action of imidacloprid on insect nicotinic acetylcholine receptors (nAChRs), we examined the roles of loop C and the loop B–C interval region in receptor interactions with imidacloprid. The P242E mutation in loop C of the Drosophila SAD subunit (the s econd α -like D rosophila nicotinic acetylcholine receptor subunit, also called Dα2 subunit) reduced imidacloprid sensitivity of the SAD-chicken β2 hybrid nAChR, whereas the E219P mutation of the α4 subunit increased the imidacloprid sensitivity of the α4β2 nAChR. Deletion of the loop B–C interval region from the SAD subunit enhanced the effect of the P242E mutation on the SADβ2 hybrid nAChR, suggesting important roles of the regions investigated in the nAChR-imidacloprid interactions.

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