As honeybees are habitually exposed to these insecticides in the field, it is crucial to understand the range of sublethal effects to effectively regulate insecticide use. While these effects are broadly associated with putative deficits in learning and memory, the possibility of neonicotinoids or sulfoximines directly affecting the neural circuitry governing flight navigation in honeybees has not previously been explored. Neonicotinoid insecticides have been linked with myriad behavioural abnormalities in managed and wild bees, including impaired navigation and foraging ( 7– 9). Sulfoxaflor is present in seed treatment mixtures that also include neonicotinoid insecticides and fungicides (e.g., VISIVIO™, Syngenta Seedcare) but no studies have examined the potential for synergy of the toxic effects of these compounds in pollinators. Sulfoxaflor and neonicotinoids like imidacloprid act on the same target, the nicotinic acetylcholine receptor (nAChR), but they are thought to be detoxified through different pathways and differ in affinity to nAChR subunits ( 5, 6). To overcome insecticide resistance, novel insecticides are continually being developed and implemented in agriculture including sulfoxaflor (a sulfoximine) that is used commercially despite known detrimental effects on bumblebee reproduction ( 4). Prophylactic use of seed treatment insecticides is prevalent, despite growing evidence of negative effects on pollinators ( 1) and birds ( 2), and putatively negligible benefits to farmers ( 3).
These findings provide a novel explanation for previously described effects of neonicotinoid insecticides on navigation and link these effects to sulfoxaflor for which there is a gap in scientific knowledge. We propose that exposure to cholinergic insecticides disrupts the honeybee’s ability to accurately encode wide-field visual motion, resulting in impaired optomotor behaviors. Exposure to sulfoxaflor led to sparse increases in neuronal apoptosis, localized primarily in the optic lobes, however there was no effect of imidacloprid. This behavioral effect correlates with altered stress and detoxification gene expression in the brain. Here, we show that sublethal exposure to two commonly used insecticides, imidacloprid (a neonicotinoid) and sulfoxaflor, results in impaired optomotor behavior in the honeybee. Neonicotinoid insecticides disrupt visual motion detection in the locust, resulting in impaired escape behaviors, but it had not previously been shown whether seed treatment insecticides disrupt wide-field motion detection in the honeybee. These effects include deficits in flight navigation and homing ability, and decreased survival of exposed worker bees. Seed treatment insecticides, including neonicotinoids and novel insecticides like sulfoxaflor, display detrimental effects on wild and managed bees, even when present at sublethal quantities. Honeybees use wide-field visual motion information to calculate the distance they have flown from the hive, and this information is communicated to conspecifics during the waggle dance. 4Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany.3Department of Biology, University of Saskatchewan, Saskatoon, SK, Canada.2Department of Zoology, University of Oxford, Oxford, United Kingdom.1Grass Laboratory, Marine Biological Laboratory, Woods Hole, MA, United States.Parkinson 1,2,3*†, Caroline Fecher 1,4† and John R.
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