Neonicotinoids in the Canadian aquatic environment: A literature review on current use products with a focus on fate, exposure, and biological effects

Anderson, Julie C.; Dubetz, Cory; Palace, Vince

doi:10.1016/j.scitotenv.2014.09.090

Cited by 326 publications

(192 citation statements)

References 77 publications

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“…In the concentration range used, 0.01 mg/ml thiacloprid proved to be the strongest blocker, while 0.1 mg/ml thiamethoxam resulted in the weakest inhibition. These results correspond with insect toxicological results, which consider thiamethoxam to be only a "moderately toxic" insecticide (Tan et al, 2007) and also by arthropod (crustacean and insect) assays (Anderson et al, 2015). We should also note, however, that thiamethoxam is the precursor of the more effective clothianidin (Benzidane et al, 2010) and likely metabolized in the treated plants or in the insects affected.…”

Section: Discussionsupporting

confidence: 87%

Neonicotinoid insecticides inhibit cholinergic neurotransmission in a molluscan (Lymnaea stagnalis) nervous system

et al. 2015

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Neonicotinoids are highly potent and selective systemic insecticides, but their widespread use also has a growing impact on non-target animals and contaminates the environment, including surface waters. We tested the neonicotinoid insecticides commercially available in Hungary (acetamiprid, Mospilan; imidacloprid, Kohinor; thiamethoxam, Actara; clothianidin, Apacs; thiacloprid, Calypso) on cholinergic synapses that exist between the VD4 and RPeD1 neurons in the central nervous system of the pond snail Lymnaea stagnalis. In the concentration range used (0.01-1 mg/ml), neither chemical acted as an acetylcholine (ACh) agonist; instead, both displayed antagonist activity, inhibiting the cholinergic excitatory components of the VD4-RPeD1 connection. Thiacloprid (0.01 mg/ml) blocked almost 90 % of excitatory postsynaptic potentials (EPSPs), while the less effective thiamethoxam (0.1mg/ml) reduced the synaptic responses by about 15 %. The ACh-evoked membrane responses of the RPeD1 neuron were similarly inhibited by the neonicotinoids, confirming that the same ACh receptor (AChR) target was involved. We conclude that neonicotinoids act on nicotinergic acetylcholine receptors (nAChRs) in the snail CNS. This has been established previously in the insect CNS; however, our data indicate differences in the background mechanism or the nAChR binding site in the snail. Here we provide the first results concerning neonicotinoid-related toxic effects on the neuronal connections in the molluscan nervous system. Aquatic animals, including molluscs, are at direct risk while facing contaminated surface waters, and snails may provide a suitable model for further studies of the behavioural/neuronal consequences of intoxication by neonicotinoids.Tihany, Hungary, July 22, 2015 Dr. Mikko Nikinmaa Editorial Office Aquatic ToxicologyDear Dr Nikinmaa, Thank you very much for your response to our manuscript submission. We gratefully thank you and our reviewers for reading the manuscript, and we appreciate all the helpful comments made.After carefully checking the Reviewers' comments we improved the manuscript on the basis of their suggestions. Please find our detailed answers to the Reviewers below. Reviewer #1:We greatly appreciate the Reviewer's comment "one of the best written manuscripts that I have reviewed" Minor points Materials and Methods How was Lymnaea saline obtained? Is this the modified HiDi saline? If not, what is HiDi?For isolating the monosynaptic components of the synaptic responses between two neurons the perfusion chamber was filled with a modified saline which reduces the polysynaptically evoked postsynaptic responses and enhances the monosynaptic component (Berry and Pentreath, 1976). This modified saline contains higher amount of divalent cations (Ca 2+ and Mg 2+ ), therefore often nicknamed as HiDi saline (Brierly et al., 1997, Sivaramakrishnan et al., 2013. We added details to the text accordingly Electrophysiological recordingThere is a Winlow 1991 anda Syed et al. 1990 (PNEC, EC50, mechanistic...) We...

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Section: Discussionsupporting

confidence: 87%

Neonicotinoid insecticides inhibit cholinergic neurotransmission in a molluscan (Lymnaea stagnalis) nervous system

et al. 2015

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“…Neonicotinoids protect against a wide range of insect species. They are effective at low concentrations and can be applied using a variety of methods [3]. They are becoming the most widespread and popular group of insecticides owing to their lower neurotoxicity for mammals [4].…”

Section: Introductionmentioning

confidence: 99%

Imidacloprid enhances liver damage in Wistar rats: Biochemical, oxidative damage and histological assessment

Chakroun¹,

Grissa²,

Ezzi³

et al. 2017

JCLM

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“…This could be explained by the fact that the primary producers are not sensitive to neonicotinic imidacloprid based on their known insecticidal type of action (Daam et al, 2013;Anderson et al, 2015). Furthermore, we noticed a bloom of floating algae and macrophytes (Lemna minor) in all microcosms including control in the present study which we, unfortunately, did not quantify.…”

Section: Figurecontrasting

confidence: 56%

Effects of insecticides on aquatic ecosystems in Bangladesh

Sumon

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Neonicotinoids in the Canadian aquatic environment: A literature review on current use products with a focus on fate, exposure, and biological effects

Cited by 326 publications

References 77 publications

Neonicotinoid insecticides inhibit cholinergic neurotransmission in a molluscan (Lymnaea stagnalis) nervous system

Neonicotinoid insecticides inhibit cholinergic neurotransmission in a molluscan (Lymnaea stagnalis) nervous system

Imidacloprid enhances liver damage in Wistar rats: Biochemical, oxidative damage and histological assessment

Effects of insecticides on aquatic ecosystems in Bangladesh

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