Initial thoughts could be that the neurotoxic drug over stimulates neuronal activity or neuronal firing. The overexpression of AChE could be a protective measure to counteract this hyper activity state.

Hi Tarek,

Thank you for your comments. Is it possible that, the result of such increased AchE level leads to reduction in Acetylcholine level in brain?  

regards,

Dear Amarendranath,

What kind of a time frame are you talking about for the effect of the toxin? fast or slow?

I would imagine that your neurotoxic drug is working as a blocker/inhibitor of Acetylcholinesterase metabolism/breakdown or its uptake or transport. Basically it could be any of these pathways that the neurotoxin is inhibiting or blocking, and therefore resulting in increased levels or accumulation of the enzyme.

Also can you tell us a bit more about the functional consequnces?

If what I said above is the case then, you would expect to see decreased acetylcholine levels and function (reduced muscle activity due to reduced ACh). This will be opposite to effects that one would  see after adding organophosphorus compounds such as nerve agents and pesticides (DDT), which inhibit acetylcholineesterase activity.

best wishes,

Refik

SLUDGE syndrome; parasympathetic poisoning.  Just a guess, but increasing acetylcholine levels by reduced clearance via inhibition of acetylcholinesterase might plausibly result in an increase in the production of the enzyme.  Similar to Refik Kanjhan but think it is resulting from the increase in acetylcholine (or more specifically overstimulation of muscarinic acetylcholine receptors) not a deficit.  http://emedicine.medscape.com/article/167726-clinical