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dc.contributor.authorMoffat, C.
dc.contributor.authorGoncalves Pacheco, J.
dc.contributor.authorSharpe, S.
dc.contributor.authorSamson, A.J.
dc.contributor.authorBollan, K.A.
dc.contributor.authorHuang, J.
dc.contributor.authorBuckland, Stephen Terrence
dc.contributor.authorConnolly, C.N.
dc.identifier.citationMoffat , C , Goncalves Pacheco , J , Sharpe , S , Samson , A J , Bollan , K A , Huang , J , Buckland , S T & Connolly , C N 2015 , ' Chronic exposure to imidacloprid increases neuronal vulnerability to mitochondrial dysfunction in the bumblebee ( Bombus terrestris ) ' , FASEB Journal , vol. 29 , no. 5 , pp. 2112-2119 .
dc.identifier.otherPURE: 202250183
dc.identifier.otherPURE UUID: c167404a-4d58-4da3-b2dc-3111dde159ef
dc.identifier.otherScopus: 84932615661
dc.identifier.otherWOS: 000354114600042
dc.identifier.otherORCID: /0000-0002-9939-709X/work/73701099
dc.descriptionThis work was funded jointly by the Biotechnology and Biological Sciences Research Council, the Department for Environment, Food and Rural Affairs, the Natural Environment Research Council, the Scottish Government, and The Wellcome Trust, under the Insect Pollinators Initiative (United Kingdom) Grant BB/ 1000313/1 (to C.N.C.).en
dc.description.abstractThe global decline in the abundance and diversity of insect pollinators could result from habitat loss, disease, and pesticide exposure. The contribution of the neonicotinoid insecticides (e.g., clothianidin and imidacloprid) to this decline is controversial, and key to understanding their risk is whether the astonishingly low levels found in the nectar and pollen of plants is sufficient to deliver neuroactive levels to their site of action: the bee brain. Here we show that bumblebees (Bombusterrestris audax) fed field levels [10 nM, 2.1 ppb (w/w)] of neonicotinoid accumulate between 4 and 10 nM in their brains within 3 days. Acute (minutes) exposure of cultured neurons to 10 nM clothianidin, but not imidacloprid, causes a nicotinic acetylcholine receptor-dependent rapid mitochondrial depolarization. However, a chronic (2 days) exposure to 1 nM imidacloprid leads to a receptor-dependent increased sensitivity to a normally innocuous level of acetylcholine, which now also causes rapid mitochondrial depolarization in neurons. Finally, colonies exposed to this level of imidacloprid show deficits in colony growth and nest condition compared with untreated colonies. These findings provide a mechanistic explanation for the poor navigation and foraging observed in neonicotinoid treated bumblebee colonies.
dc.relation.ispartofFASEB Journalen
dc.rights© The author(s). This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International (CC BY 4.0) ( which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.en
dc.subjectNicotinic acetylcholine receptorsen
dc.subjectNeuronal cultureen
dc.subjectQH301 Biologyen
dc.subjectQA Mathematicsen
dc.titleChronic exposure to imidacloprid increases neuronal vulnerability to mitochondrial dysfunction in the bumblebee (Bombus terrestris)en
dc.typeJournal articleen
dc.description.versionPublisher PDFen
dc.contributor.institutionUniversity of St Andrews.School of Mathematics and Statisticsen
dc.contributor.institutionUniversity of St Andrews.Marine Alliance for Science & Technology Scotlanden
dc.contributor.institutionUniversity of St Andrews.Scottish Oceans Instituteen
dc.contributor.institutionUniversity of St Andrews.St Andrews Sustainability Instituteen
dc.contributor.institutionUniversity of St Andrews.Centre for Research into Ecological & Environmental Modellingen
dc.description.statusPeer revieweden

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