Botulism toxin acts via proteases that cleave SNARE and prevent acetylcholine release at the neuromuscular junction (FA2020 p132). Thus, it does not directly affect the post-synatpric muscle cell. If you add external acetylcholine, you would still have a completely normal response. This eliminates all but two answers.

The end plate potential (EPP) would be affected by botulism toxin because the end plate potential is the change in voltage that occurs at the postsynaptic muscle motor endplate after an action potential in the motor neuron axon triggers release of many acetylcholine vesicles. Normally, an action potential in the motor neuron will cause influx of calcium that leads to fusion of Ach vesicles (requiring SNARE) and exocytosis, releasing large quantities of Ach into the synapse which can then bind and trigger an EPP in the muscle. With botulism, fusion of the Ach vesicles is inhibited so less Ach is released and the EPP is blunted. Notably, the voltage is the same as the mEPP which is the voltage after random occurrence of Ach release (see below).

A miniature end plate potential (mEPP) is the voltage change that occurs when one vesicle of acetylcholine is released. These occur randomly. mEPP would not be affected by botulism toxin because it is the produce of random fusion of a vesicle which could still occur after administration of botulism toxin.

Here is an image reminding the difference between EPP and mEPP.

Although botulism blocks ACh release, it wouldn't have effects on mpp and the response to exogenous ACh provided to the synaptic junction. The potentials would be the same as it would normally be. The epp difference was disclaimed in the question stem.