The mechanism of action of erabutoxin b is not completely known; however it is believed to act at the acetylcholine receptor like that of cobratoxin and curare. When an organism, usually a fish but sometimes a human, is bitten by Laticauda semifasciata erabutoxin b binds to the nicotinic acetylcholine receptor on the motor end plate and blocks it indefinitely. Normally when acetylcholine binds to this same receptor an ion channel is opened on the motor end plate and an influx of Na+ cause the depolarization of the end plate. If this depolarization initiates an action potential, a skeletal muscle contraction is the result. Erabutoxin b binds to the acetylcholine receptor and causes a neuromuscular blockade between the phrenic nerve and the diaphram. Paralysis of the diaphram occurs resulting in death by respiratory arrest. The following figure[6] shows a schematic view of the acethylcholine receptor in action.

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