> If insect response to neonicotinoids is similar to the nicotinoid response by vertebrates (and why not), 

Why not is because they are insects, not mammals. There is absolutely no reason to suppose that it would be the same

> the toxic threshold would continue to be reached in spite of any increased threshold (adaptation). 

I think the use of the word adaptation is unhelpful here. I believe you are referring to the development of tolerance.

> However, if bees adapt as verts do, they will become "addicts" and tolerate much higher doses 

This is erroneous. Organisms develop tolerance to plenty of substances. Addiction is a completely separate phenomenon (which may also include tolerance).

> At that point of high tolerance, taking the drug AWAY is more "harmful" in the short term than continuing to feed the addiction.  

This is a non-sequitir. We don't know if insects become addicted to pesticides. 

> I just don't know if insects react the same way.  

Very small changes on the molecule make enormous differences. Neonicotinoids are not the same as nicotine. Take the example of ethanol and methanol. Very similar molecules; very different properties. The neonics were developed precisely to exploit the fact that they do NOT produce the same effects in mammals as insects. 

> Neonicotinoid insecticides display excellent selectivity profiles that are largely attributable to specificity for insect versus mammalian nAChRs  (Nicotinic acetylcholine receptors). 

> Neonicotinoids have little or no effect on the vertebrate peripheral nAChR. The mammalian nAChR is a potential target for therapeutic agents for analgesia, neurodegenerative diseases, cognitive dysfunction, schizophrenia, depression, and anxiety
 
> The insecticidal activity of the neonicotinoids is due to their action as insect nAChR agonists.

NEONICOTINOID INSECTICIDE TOXICOLOGY:
Mechanisms of Selective Action
Motohiro Tomizawa and John E. Casida
Annu. Rev. Pharmacol. Toxicol. 2005. 45:247–68

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