Answer:
When a poison prevents the release of acetylcholine, at the myoneural junction occurs that sodium and potassium gates on the motor end plate will not open.
Step-by-step explanation:
In cholinergic transmission, acetylcholine released by the presynaptic neuron binds to a specific receptor in the postsynaptic terminal. The effect of acetylcholine on its receptor produces the opening of sodium and potassium gates, whose exchange determines the transmembrane action potential.
If an acetylcholine release inhibitor —like a poison— is ingested, the absence of acetylcholine at the myoneural junction prevents the opening of the sodium and potassium gates. This results in the function of the effector, the muscle, not being performed.
The other options are not correct because obviously the action of acetylcholine is the opening of the sodium and potassium gates, not their closing.