Chronic exposure to neonicotinoids increases neuronal vulnerability to mitochondrial dysfunction in the bumblebee (Bombus terrestris)

Christopher Moffat, Joao Goncalves Pacheco, Sheila Sharp, Andrew J. Samson, Karen A. Bollan, Jeffrey Huang, Stephen T. Buckland, Christopher N. Connolly

Research output: Contribution to journalArticle

50 Citations (Scopus)
286 Downloads (Pure)

Abstract

The 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 (Bombus terrestris 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.

Original languageEnglish
Pages (from-to)2112-2119
Number of pages8
JournalFASEB Journal
Volume29
Issue number5
Early online date29 Jan 2015
DOIs
Publication statusPublished - May 2015

Keywords

  • Neuronal culture
  • Nicotinic acetylcholine receptors

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    24 Feb 2015

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