Pyrethroids and Nectar Toxins Have Subtle Effects on the Motor Function, Grooming and Wing Fanning Behaviour of Honeybees (Apis mellifera).
Sodium channels, found ubiquitously in animal muscle cells and neurons, are one of the main target sites of many naturally-occurring, insecticidal plant compounds and agricultural pesticides. Pyrethroids, derived from compounds found only in the Asteraceae, are particularly toxic to insects and have been successfully used as pesticides including on flowering crops that are visited by pollinators. Pyrethrins, from which they were derived, occur naturally in the nectar of some flowering plant species. We know relatively little about how such compounds--i.e., compounds that target sodium channels--influence pollinators at low or sub-lethal doses. Here, we exposed individual adult forager honeybees to several compounds that bind to sodium channels to identify whether these compounds affect motor function. Using an assay previously developed to identify the effect of drugs and toxins on individual bees, we investigated how acute exposure to 10 ng doses (1 ppm) of the pyrethroid insecticides (cyfluthrin, tau-fluvalinate, allethrin and permethrin) and the nectar toxins (aconitine and grayanotoxin I) affected honeybee locomotion, grooming and wing fanning behaviour. Bees exposed to these compounds spent more time upside down and fanning their wings. They also had longer bouts of standing still. Bees exposed to the nectar toxin, aconitine, and the pyrethroid, allethrin, also spent less time grooming their antennae. We also found that the concentration of the nectar toxin, grayanotoxin I (GTX), fed to bees affected the time spent upside down (i.e., failure to perform the righting reflex). Our data show that low doses of pyrethroids and other nectar toxins that target sodium channels mainly influence motor function through their effect on the righting reflex of adult worker honeybees.
Centre for Behaviour and Evolution, Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, United Kingdom; School of Biology, Newcastle University, Newcastle upon Tyne, United Kingdom.
Caitlin J
CJ
Oliver
Centre for Behaviour and Evolution, Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, United Kingdom; School of Biology, Newcastle University, Newcastle upon Tyne, United Kingdom.
Samantha
S
Softley
Centre for Behaviour and Evolution, Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, United Kingdom; School of Biology, Newcastle University, Newcastle upon Tyne, United Kingdom.
Sally M
SM
Williamson
Jodrell Laboratory, Royal Botanic Gardens, Kew, Surrey, United Kingdom; Natural Resources Institute, University of Greenwich, Chatham, United Kingdom.
Philip C
PC
Stevenson
Centre for Behaviour and Evolution, Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, United Kingdom.
Geraldine A
GA
Wright
D000157:Aconitine / Q000633:toxicity; D000818:Animals; D001516:Bees; D001522:Behavior, Animal / Q000187:drug effects; D004224:Diterpenes / Q000633:toxicity; D006120:Grooming / Q000187:drug effects*; D007306:Insecticides / Q000633:toxicity; D008124:Locomotion / Q000187:drug effects*; D009570:Nitriles / Q000633:toxicity; D026023:Permethrin / Q000633:toxicity; D057048:Plant Nectar / Q000633:toxicity*; D011722:Pyrethrins / Q000633:toxicity*; D014921:Wings, Animal / Q000187:drug effects / Q000502:physiology
D004224:Diterpenes; D007306:Insecticides; D009570:Nitriles; D057048:Plant Nectar; D011722:Pyrethrins; C034227:fluvalinate; D026023:Permethrin; C052570:cyfluthrin; C001311:grayanotoxin I; D000157:Aconitine