Neonicotinoid Insecticides: Molecular Targets, Resistance, and Toxicity

Abstract

Neonicotinoids have been used to protect crops and animals from insect pests since the 1990s, but there are concerns regarding their adverse effects on nontarget organisms, notably on bees. Enhanced resistance to neonicotinoids in pests is becoming well documented. We address the current understanding of neonicotinoid target site interactions, selectivity, and metabolism not only in pests but also in beneficial insects such as bees. The findings are relevant to the management of both neonicotinoids and the new generation of pesticides targeting insect nicotinic acetylcholine receptors.

Neonicotinoids disrupt memory, circadian behaviour and sleep

“…They share a mechanism of action, being agonists of nicotinic acetylcholine receptors (nAChR), the main neurotransmitter in the insect nervous system. They also display target site cross-resistance in pests, diminishing their effectiveness as insecticides and unfortunately encouraging application of increasing concentrations 7,17 . They were branded safe compared to previous insecticides because they do not act on mammalian nAChRs 7,17 .…”

“…They also display target site cross-resistance in pests, diminishing their effectiveness as insecticides and unfortunately encouraging application of increasing concentrations 7,17 . They were branded safe compared to previous insecticides because they do not act on mammalian nAChRs 7,17 . However, few precursive safety tests were performed on beneficial insects, for which neonicotinoids are now known to be potent neurotoxins with well-documented lethal and sub-lethal effects 11,15,17,18,19 .…”

“…Concentrations as low as 1 µg/L (or 1 part per billion (ppb)) can cause significant behavioural effects due to the high potency of neonicotinoids, such as reduced foraging motivation in the bumblebee Bombus terrestris 28 . The potential sub-lethal effects of neonicotinoids are very far-reaching because of the central role of nAChR in synaptic neurotransmission in the insect brain 7,17 .…”

“…Neonicotinoids cause this ligand-gated ion channel to open, thereby depolarising the neuron and increasing excitability. Prolonged exposure to the depolarising agonist may result in depolarising block, through voltage inactivation of voltage-sensitive Na + channels required for action potential firing and nAChR desensitization 7,29 . This effect could have pronounced effects on memory formation and consolidation, which are critical for effective foraging in many pollinating insects.…”

The neonicotinoid insecticide imidacloprid disrupts bumblebee foraging rhythms and sleep

“…The most common insecticides worldwide are neonicotinoids, global sales of which are worth US$1 billion/year [2,10]. Neonicotinoids have the same mechanism of action, being agonists of nicotinic acetylcholine receptors (nAChR), the main neurotransmitter system in the insect nervous system, and share target site cross-resistance [11]. They were branded safe compared to their predecessors because they do not act on mammalian nAChRs [2,11].…”