Chronic exposure to neonicotinoids increases neuronal vulnerability to
mitochondrial dysfunction in the bumblebee (Bombus terrestris).
Moffat C1, Pacheco JG1, Sharp S1, Samson AJ1, Bollan KA1, Huang J1, Buckland
ST1, Connolly CN2.

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.
C FASEB.

More here:
http://www.ncbi.nlm.nih.gov/pubmed/25634958

(paywall)

Kind regards,

Ghislain De Roeck
Belgium.

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