I'm sorry this line of study out of my interest. but may be the following paper useful to you:

Shellfish Toxins Targeting Voltage-Gated Sodium Channels

http://www.mdpi.com/1660-3397/11/12/4698/htm

Maybe this can help you 

”In vitro models for neurotoxicology research“

http://pubs.rsc.org/en/content/articlelanding/2015/tx/c4tx00043a#!divAbstract

The case of botulinum toxin illustrates the advantage of the degradation approach. The most potent form of this toxin, which causes muscle paralysis, has a half-life in the body of about 3 months. Although an inhibitor of the toxin would be able to suppress toxicity in the short term, elimination of the toxin is obviously a preferable therapeutic approach. However, the Boc3Arg moiety is large (almost 500 daltons in mass), and large molecules often have poor pharmacokinetic properties that limit their use as drugs. So,

appending it to an existing inhibitor could potentially worsen that inhibitor’s pharmacokinetic

properties. 

http://magz.elibraries.eu/ul/1826/Nature%20Magazine%207407%20-%202012-07-19.pdf