The resulting movement of sodium ions produces the action potential causing the muscles to contract. At this point, an enzyme called acetylcholinesterase then cleaves the neurotransmitter, allowing the sodium channel to return eventually to its resting state, and hence the muscle can relax. Anatoxin also binds the NAChR to produce an action potential, but cannot be cleaved by the enzyme. The sodium channel is essentially locked open, and the muscles become over-stimulated and become fatigued and then paralysed. When respiratory muscles become affected, convulsions occur due to a lack of oxygen supply to the brain.
Suffocation is the final result a few minutes after ingestion of the toxin.
Despite its poisonous nature, however, anatoxin and many related man-made analogues have found widespread use in medicine and for pharmacological applications. Since it binds the nicotinic acetylcholine receptor irreversibly, it is an excellent means of studying this receptor, and also the mechanisms of neuromuscular action. Modified analogues are being used in order to further elucidate the receptor sub-types, and this research may lead to the development of new drugs which have none of the toxicity associated with anatoxin itself, but which act merely as acetylcholine replacement candidates. For example, the neurodegenerative disorder, Alzheimer's disease is associated with an inability of neurons to produce acetylcholine. Using the neurotransmitter itself as a therapy would not work since it is not long-lived enough.