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Neurosci Lett. 2002 Mar 15;321(1-2):13-6.

The insecticide imidacloprid is a partial agonist of the nicotinic receptor of honeybee Kenyon cells.

Author information

1
Laboratoire de Neurobiologie de l'Insecte, Université Paul Sabatier, 118 route de Narbonne, F-31062 Toulouse, France. patrice_deglise@yahoo.fr

Erratum in

  • Neurosci Lett 2002 May 10;324(1):86.

Abstract

The main targets of the insecticide imidacloprid are neuronal nicotinic acetylcholine receptors (nAChRs) within the insect brain. We tested the effects of imidacloprid on ligand-gated ion channels of cultured Kenyon cells of the honeybee, Apis mellifera. Kenyon cells build up the mushroom body neuropils, which are involved in higher order neuronal processes such as olfactory learning. We measured whole-cell currents through nicotinic and gamma-aminobutyric acid (GABA) receptors using patch-clamp techniques. Pressure applications of imidacloprid elicited inward currents, which were irreversibly blocked by alpha-bungarotoxin. Imidacloprid was a partial nicotinic agonist, since it elicited only 36% of ACh-induced currents and competitively blocked 64% of the peak ACh-induced currents. GABA-induced currents were partially blocked when imidacloprid was coapplied and this block was independent upon activation of nAChRs. Our results identify the honeybee nAChR as a target of imidacloprid and an imidacloprid-induced inhibition of the insect GABA receptor.

PMID:
11872245
DOI:
10.1016/s0304-3940(01)02400-4
[Indexed for MEDLINE]

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