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Selective actions of insecticides on desensitizing and non‐desensitizing nicotinic acetylcholine receptors in cockroach ( Periplaneta americana ) neurons
Author(s) -
Salgado Vincent L
Publication year - 2021
Publication title -
pest management science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.296
H-Index - 125
eISSN - 1526-4998
pISSN - 1526-498X
DOI - 10.1002/ps.6396
Subject(s) - nicotinic agonist , periplaneta , nicotinic antagonist , neonicotinoid , acetylcholine receptor , pharmacology , ganglion type nicotinic receptor , imidacloprid , alpha 4 beta 2 nicotinic receptor , acetylcholine , mecamylamine , chemistry , nicotinic acetylcholine receptor , allosteric regulation , receptor , clothianidin , american cockroach , cockroach , agonist , biology , biochemistry , thiamethoxam , ecology , pesticide
BACKGROUND Insect desensitizing nicotinic acetylcholine (nAChD) receptors are desensitized by low concentrations of agonists, including neonicotinoid insecticides, but are essentially insensitive to spinosyns, while non‐desensitizing nicotinic acetylcholine (nAChN) receptors are selectively activated by spinosyns and relatively insensitive to neonicotinoids. RESULTS The single‐electrode voltage‐clamp technique was used to measure the actions of newer nicotinic insecticides dinotefuran, sulfoxaflor, triflumezopyrim, spinetoram and GS‐ω/k‐hexatoxin‐Hv1a on cockroach neuronal nAChD and nAChN currents. Like imidacloprid and clothianidin, newer orthosteric nicotinic agonist insecticides dinotefuran and sulfoxaflor act by desensitizing nAChD receptors. The mesoionic insecticide triflumezopyrim selectively inhibited nAChD current with an half maximal inhibitory concentration (IC 50 ) of 1.2 nmol L −1 , with no activation. Unlike other Group 4 insecticides, it did not activate nAChN current, but inhibited it with an IC 50 of 3.8 μmol L −1 , indicating that the compound is a true antagonist. Spinosad and the spinosyn‐derived insecticide spinetoram potently and selectively activated nAChN receptors. GS‐ω/k‐hexatoxin‐Hv1a had no effect on nAChN currents and it had a complex action on nAChD currents, inhibiting at sub‐nanomolar concentrations and causing some activation and enhancement of ACh‐evoked currents at 30 nmol L −1 and above. Some cells express GS‐ω/k‐hexatoxin‐Hv1a‐resistant nAChD receptors. CONCLUSIONS Nicotinic acetylcholine receptor competitive modulators (IRAC Group 4) and nicotinic acetylcholine receptor allosteric modulators, site II (hexatoxins, IRAC Group 32) are selective for nAChD receptors, while nicotinic acetylcholine receptor allosteric modulators, site I (spinosyns, IRAC Group 5) are selective for nAChN receptors. It is proposed that IRAC Groups 5 and 32 be re‐named non‐desensitizing nicotinic acetylcholine receptor allosteric modulators and desensitizing nicotinic acetylcholine receptor allosteric modulators, respectively. © 2021 Society of Chemical Industry.