Citation from "Acetylcholinesterase in honey bees (Apis mellifera) exposed
to neonicotinoids, atrazine and glyphosate: lanoratory and fiels
experiments" Monique Boily et al. (2012):

"Neonicotinoids and their metabolites are agonists of acetylcholine (Nauen
et al. 2001). They bind to the post-synaptic nicotinic receptors nAChERs
triggering a continuous signal leading to the death of the insect? Their
high efficiency is attributed to the irreversible link with the nAChERs
receptors (Thany 2009) recognized as the most abundant in insects (Gauthier
2010) and the partial inhibition of u-aminobutyric acid (GABA) receptors
known to protect the cell from overstimulation (Déglise et al. 2002)."

(Thany 2009)
http://dx.doi.org/10.1016/j.neuro.2009.06.013

"Agonist actions of clothianidin on synaptic and extrasynaptic nicotinic
acetylcholine receptors expressed on cockroach sixth abdominal ganglion."


Abstract

Clothianidin is new neonicotinoid insecticide acting selectively on insect
nicotinic acetylcholine receptors (nAChRs). Its effects on nAChRs expressed
on cercal afferent/giant interneuron synapses and DUM neurons have been
studied using mannitol-gap and whole-cell patch-clamp techniques,
respectively. Bath-application of clothianidin-induced dose-dependent
depolarizations of cockroach cercal afferent/giant interneuron synapses
which were not reversed after wash-out suggesting a strong desensitization
of postsynaptic interneurons at the 6th abdominal ganglion (A6). Clothinidin
activity on the nerve preparation was characterized by an increased firing
rate of action potentials which then ceased when the depolarization reached
a peak. Clothianidin responses were insensitive to all muscarinic
antagonists tested but were blocked by co-application of specific nicotinic
antagonists methyllicaconitine, α-bungarotoxin and d-tubocurarine.

In a second round of experiment, clothianidin actions were tested on DUM
neurons isolated from the A6. There was a strong desensitization of nAChRs
which was not affected by muscarinic antagonists, pirenzepine and atropine,
but was reduced with nicotinic antagonist α-bungarotoxin. In addition,
clothianidin-induced currents were completely blocked by methyllicaconitine
suggesting that (1) clothianidin acted as a specific agonist of nAChR
subtypes and (2) a small proportion of receptors blocked by MLA was
insensitive to α-bungarotoxin. Moreover, because clothianidin currents were
blocked by d-tubocurarine and mecamylamine, we provided that clothianidin
was an agonist of both nAChRs: imidacloprid-sensitive nAChR1 and
-insensitive nAChR2 subtypes.


Kind regards,

Ghislain De Roeck,
Belgium.

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