The question troubling Ghislain is whether or not imidacloprid binds irreversibly to ACh receptors.

Before I answer Randy's questions about the paper Ghislain found, I'd like to point you to another source that says binding by imidacloprid to AChR in insects is "irreversible".   According to the National Pesticide Information Center, imidacloprid binding to insect ACh receptors is irreversible.

http://npic.orst.edu/factsheets/imidacloprid.pdf

Check it out.

Now what does "irreversible" mean?  In a normal body, if the introduced chemical binds to the receptor and does not let go, and there is no enzyme around to degrade it, that is to all intents and purposes "irreversible".  When biochemists do binding studies on membrane preparations in order to determine receptor binding affinities, they use standards like alpha bungarotoxin to see if they can "displace" the chemical of interest...this is called a "competitive binding assay".  This way they can get an idea of which chemicals bind most aggressively to the receptors compared to others.  I'm not in that field, but the gist of it is that the stronger the bond between the chemical and the receptor, the harder it is to displace the molecule from the receptor using one of the well-characterized standard agonists.

***Note that displacement of any of these chemical agonists is done using another chemical agonist also not found in the synapse, or in the whole animal either for that matter.  Thus, under normal conditions, binding is "irreversible"....there's nothing there to displace the compound in the living insect, out in the field, once it has reached the synapse.  Hence, the National Pesticide Information Center says that imidacloprid binds irreversibly.

If Dr. Casida told Randy that binding was reversible, I wonder what Randy's exact question was?  Perhaps it was a conversation held in the context of these types of competitive binding assays.  It would be possible to dislodge IMI from a receptor in a lab.  I don't think the insect can do it alone, however, and the National Pesticide Information Center agrees on this point.  (There are ways neurons adapt and some evidence insects can do this, however...another topic!)

Now as to the critique of the paper, Randy, I don't have access to it as I use the Cornell library and they don't subscribe to "Pflanzenschutz-Nachrichten Bayer" anymore.  So I'll have to go with just your comments and try to deal with the paper second-hand.

Frozen or fresh, the experiment determining reversibility would most likely be as I described above, so not a problem to do a dissociated membrane experiment.

If they used a whole head homogenate of Stomoxys to get their membrane preps there would be other compounds in there, certainly, including native acetylcholinesterase.  So your concern that acetylcholine could displace the neonics but was probably diminished because of acetylcholinesterase is valid, but doesn't matter, because it's already established that the neonics displace acetylcholine on the AChR...that's how they work!

When they say that the IMI blocks the receptors, they mean it blocks the function of the receptor.  It usually is blocked in the "open" position, depolarizing the cell.

Interesting about the finding that binding affinity dropping off with increased IMI concentration.  Would have to actually read the paper to figure that out, I think.

If you can send me the paper Randy I will try to answer the questions more thoroughly.

Christina

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