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Acetylcholine is a neurotransmitter that mainly interacts with receptors at the NMJ in cardiovascular muscle (parasympathetic innervation) and skeletal muscle.

It wouldn't prevent an action potential from occurring, because an action potential is a function of a VGNaC opening, and generally doesn't have much to do with neurotransmitters.

It wouldn't maintain a resting potential, because that is the function of various ion pumps and channels around the neuronal membrane.

It wouldn't directly decrease the rate of action potentials, because that is a function of many other biochemical processes I won't bore you with.

Neurotransmitters are released as a function of synaptic fusion via $Ca^(2+)$ influx near the active zone of the presynaptic neuron. Acetylcholine would bind to various receptors (either inhibitory or excitatory) on the postsynaptic neuron's dendrites to create either EPSP's or initiate biochemical mechanisms namely starting with G-proteins.

Hence, the answer is probably $"A"$ (although it is in crude language).

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