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 second alpha-like Drosophila nicotinic acetylcholine receptor subunit, also called Dalpha2 subunit) reduced imidacloprid sensitivity of the SAD-chicken beta2 hybrid nAChR, whereas the E219P mutation of the alpha4 subunit increased the imidacloprid sensitivity of the alpha4beta2 nAChR. Deletion of the loop B-C interval region from the SAD subunit enhanced the effect of the P242E mutation on the SADbeta2 hybrid nAChR, suggesting important roles of the regions investigated in the nAChR-imidacloprid interactions.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Acetylcholine / pharmacology
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Animals
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Chickens
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Dose-Response Relationship, Drug
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Drosophila
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Imidazoles / pharmacology*
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Insecta / drug effects*
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Insecticides / pharmacology*
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Membrane Potentials / drug effects
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Mutagenesis, Site-Directed
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Neonicotinoids
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Nitro Compounds
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Oocytes
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Patch-Clamp Techniques
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Plants*
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Protein Structure, Quaternary
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Protein Subunits / chemistry
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Protein Subunits / metabolism*
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Receptors, Nicotinic / chemistry
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Receptors, Nicotinic / drug effects
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Receptors, Nicotinic / metabolism*
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Recombinant Fusion Proteins / metabolism
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Sequence Alignment
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Structure-Activity Relationship
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Transfection
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Xenopus laevis
Substances
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Imidazoles
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Insecticides
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Neonicotinoids
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Nitro Compounds
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Protein Subunits
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Receptors, Nicotinic
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Recombinant Fusion Proteins
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imidacloprid
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Acetylcholine