A hypothesis to account for the selective and diverse actions of neonicotinoid insecticides at their molecular targets, nicotinic acetylcholine receptors: Catch and release in hydrogen bond networks

Makoto Ihara, Masaru Shimomura, Chiharu Ishida, Hisashi Nishiwaki, Miki Akamatsu, David B. Sattelle, Kazuhiko Matsuda

    Research output: Contribution to journalArticlepeer-review

    Abstract

    The low mammalian toxicity of neonicotinoid insecticides has been shown to be attributable, at least in part, to their selective actions on insect nicotinic acetylcholine receptors (nAChRs). There are multiple nAChRs in insects and a wealth of neonicotinoid chemicals. Studies to date have discribed a wide range of effects on nAChRs, notably partial agonist, super agonist and antagonist actions. Both the diversity of the neonicotinoid actions and their selectivity for insect over vertebrate nAChRs are the result of physicochemical and steric interactions at their molecular targets (nAChRs). In such interactions, the formation and breakage of hydrogen bond (HB) networks plays a key role. Therefore the loss or gain of even a single HB resulting from either structural changes in neonicotinoids, or the amino acid sequence of a particular nAChR subunit, could result in a drastic modification of neonicotinoid actions. In addition to the amino acid residues, the backbone carbonyl of nAChRs may also be involved in the formation of HB networks with neonicotinoids. © 2007 Springer-Verlag.
    Original languageEnglish
    Pages (from-to)47-51
    Number of pages4
    JournalInvertebrate Neuroscience
    Volume7
    Issue number1
    DOIs
    Publication statusPublished - Mar 2007

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