The major sources of reactivity are from non proteinacious toxin molecules, acetylcholine, and a toxin that affects neuromuscular transmission.
Fmarini: I was wondering if you knew any more details concerning how it affects the Acetylcholine neurotransmitters. Anything that affects ACh, has the potential to be quite serious. ACh is the messenger at every junction between a motor neruon and a skeletal muscle. Basically, when ACh is released by the axons on of one nerve, and recieved by the dendrites of another nerve, it causes the muscle to contract. There are 3 main possibilities that could happen depending on how the ACh is affected by the lionfish venom.
#1 - It can occupy and block the receptor sites on a recieving neuron which will prevent ACh from being transmitted, in turn not allowing muscles to contract, which is basically being paralyzed. It's the type of stuff indian tribes use to hunt...they put a poison, Curare, on their darts which blocks receptor sites causing the animal to become paralyzed.
#2 - Another "option" is that it can block the release of ACh on the sending neuron which would have the same affect as blocking the recieving neuron. An example of this would be from Botulin poisining which can form in the inproper canning of canned foods.
#3 - The third option and most dangerous would be if it causes a synaptic flood of ACh from the sending neuron to the recieving neuron. In this case, black widow spider venom is a good example. It "impersonates" ACh and "overflows" the recieving neuron with what it thinks is ACh...thus causing violent muscle contractions, convulsions, and POSSIBLE death.
My basic question to you is do you know if it acts as an Agonist (mimics the neurotransmitter), or an Antagonist ( blocks neurotransmitter). I don't usually post in the aggresive forum having a reef tank but I felt your response was left open-ended without specifying the exact affect on the ACh.
Sorry for the neuroscience lecture, I tried to keep it in lehman's terms as mush as possible.