Hi Philipp,

First of all, imidacloprid is a systemic chloro-nicotinyl insecticide that causes a blockage in the nicotinergic neuronal pathway in insects, resulting in the accumulation of the acetylcholine neurotransmitter, causing the paralysis and death of the insect. Accordingly, it is clear that imidacloprid acts as an insect neurotoxin; so I think that it is obvious to say (your statement) that the best you could find were studies about changes in brain metabolism. However, several insecticide active ingredients have other modes of action: some of them are insect growth regulators (e.g. of active ingredients: buprofezin, Teflubenzuron, pyriproxyfen,…), others are Acetylcholinesterase (AChE) inhibitors (e.g.: aldicarb, bendiocarb, malathion, methidathion,…), and others (this is in response to your question) are mitochondrial complexes electron transport inhibitors, belonging to the Metabolic processes / Energy production insecticide group (e.g.: rotenone, sulfuryl fluoride, tebufenpyrad,…), etc...

As suggestion, you can check out the three following links (with useful references) stating different modes (sites) of action of active ingredients (including those inducing metabolic changes in insects), with some examples of target insect pests:

http://www.entmclasses.umd.edu/peap/leaflets/pil43.pdf

https://extension.arizona.edu/sites/extension.arizona.edu/files/resourcefile/resource/marcop/IRAC%20MOA%20brochure_v4%202_Oct10.pdf

http://znaturforsch.com/ac/v57c/s57c1028.pdf

Good luck!

Cheers

Dear Philipp,

the impact of stressors in organisms can lead to situations like the one you reported. Although no variance in food consumption is observed for exposed organisms, the activation of the detoxification pathways will require energy and a decrease in weight is then observed. I have observed this effect in isopods exposed to dimethoate where a significant decrease of carbohydrates was observed. You can find several studies with similar results also for isopods, since mine is not yet published.

Hi Philipp,

First of all, imidacloprid is a systemic chloro-nicotinyl insecticide that causes a blockage in the nicotinergic neuronal pathway in insects, resulting in the accumulation of the acetylcholine neurotransmitter, causing the paralysis and death of the insect. Accordingly, it is clear that imidacloprid acts as an insect neurotoxin; so I think that it is obvious to say (your statement) that the best you could find were studies about changes in brain metabolism. However, several insecticide active ingredients have other modes of action: some of them are insect growth regulators (e.g. of active ingredients: buprofezin, Teflubenzuron, pyriproxyfen,…), others are Acetylcholinesterase (AChE) inhibitors (e.g.: aldicarb, bendiocarb, malathion, methidathion,…), and others (this is in response to your question) are mitochondrial complexes electron transport inhibitors, belonging to the Metabolic processes / Energy production insecticide group (e.g.: rotenone, sulfuryl fluoride, tebufenpyrad,…), etc...

As suggestion, you can check out the three following links (with useful references) stating different modes (sites) of action of active ingredients (including those inducing metabolic changes in insects), with some examples of target insect pests:

http://www.entmclasses.umd.edu/peap/leaflets/pil43.pdf

https://extension.arizona.edu/sites/extension.arizona.edu/files/resourcefile/resource/marcop/IRAC%20MOA%20brochure_v4%202_Oct10.pdf

http://znaturforsch.com/ac/v57c/s57c1028.pdf

Good luck!

Cheers

Thank you both!

Yes, my research team did some work about this in mosquitoes. A look at my publication list for more details.

Best

Please check these papers on imidacloprid effects (some effects on growth , feeding and respiration rates)

:http://www.sciencedirect.com/science/article/pii/S0045653509012934

http://www.sciencedirect.com/science/article/pii/S0166445X09001428

http://www.sciencedirect.com/science/article/pii/S0166445X09001428

you also have this paper on imidacloprid:

Molecular mechanisms associated with increased tolerance to the neonicotinoid insecticide imidacloprid in the dengue vector Aedes aegypti

http://dx.doi.org/10.1016/j.aquatox.2012.09.010

Dear Philipp,

see on Research Gate some of my articles, where impact of imidacloprid on digestive enzymes activities and intestinal absorption was studied.

I mean here:

1. Digestive enzymes activity in subsequent generations of Cameraria ohridella larvae harvested from horse chestnut trees after treatment with imidacloprid

Dominika Stygar, Katarzyna Michalczyk, Bogdan Dolezych, Miroslaw Nakonieczny, Pawel Migula, Maria Zaak, Tomasz Sawczyn, Iwona Karcz-Socha, Michal Kukla, Krystyna Zwirska-Korczala, Rafal Buldak

2. Within and between seasonal changes of detoxifying capabilities of Cameraria ohridella (Lepidoptera: Gracillariidae) larvae

Maria Zaak, Pawel Migula, Dominika Stygar, Bogdan Dolezych, Katarzyna Michalczyk

3. Alteration of carbohydrates metabolism and midgut glucose absorption in Gromphadorhina portentosa after subchronic exposure to imidacloprid and fenitrothion.

Tomasz Sawczyn, Bogdan Dolezych, Marcin Klosok, Maria Augustyniak, Dominika Stygar, Rafal J Buldak, Michal Kukla, Katarzyna Michalczyk, Iwona Karcz-Socha, Krystyna Zwirska-Korczala

Best regards

Bogdan

Dear Philip

I suggest that you find a publish as below Title, it can be useful to you:

Sharma, R., Komatsu, S. and Noda, H. 2004. Proteomic analysis of brown plant hopper: application to the study of carbamate toxicity. Insect Biochemistry and Molecular Biology, 34: 425-432

Dear Philip

I hereby forward you a reference on: Energetic Cost of Subacute Chlorpyrifos Intoxication in the German Cockroach (Dictyoptera: Blattellidae)

Author(s): Søren Achim Nielsen, Karl-Martin Vagn Jensen, Michael Kristensen,

and Peter Westh

Source: Environmental Entomology, 35(4):837-842. 2006.

Best

Karl-Martin

Thank you all for your support!

Agree with Nuno that energy spent in detoxification is one of the reasons for the decrease in weight of the organisms even if they feed at normal rates. In addition, the agonist neonicotinoids produce stress by activating continuously the neurones in the central nervous system. Such an stress may imply a waste of energy, which must come from the food intake.