An end plate potential is the change in membrane potential induced by the action of multiple mini end plate potentials (MEPP).
In resting muscle, there is occasional leak of single acetylcholine vesicles. This produces a very small but notable electrical response in the muscle (~0.5mV). The response generated by one acetylcholine-containing vesicle represents the smallest possible depolarization which can be induced in a muscle ie. represents a MEPP.
If multiple vesicles are released, the electrical response is correspondingly larger. The summation of multiple MEPPs produces an End Plate Potential (EPP).
In a normal muscular contraction, ~150 acetylcholine vesicles are released. Therefore, the EPP is 150 times greater than the MEPP.
Because the electrical depolarization of a muscle must be an integer multiple of the MEPP, muscle depolarization is considered quantal.
Stated another way: because you cannot have 0.5 of a vesicle released (ie the vesicle contents are completely exocytosed or not at all), the depolarization of a muscle must be a multiple of the depolarization caused by one single vesicle being exocytosed.
(1) Myasthenia Gravis : In Myasthenia Gravis, there is autoimmune destruction of post synaptic acetylcholine receptors. Because there are less receptors, it is less probable that all the acetylcholine within a vesicle will find a receptor to bind to. Consequently, MEPP is decreased in myasthenia. As EPP is the summation of MEPPs, it is also decreased.
(2) Lambert Eaton Syndrome: In Lambert Eaton syndrome, presynaptic calcium channels responsible for facilitating vesicle exocytosis are subject to autoimmune destruction. Because less calcium influx occurs, less vesicles are exocytosed. The MEPP remains identical to a normal person because once a vesicle is released, its effect on the post-synaptic receptors is not affected by the disease. However, the EPP is lower relative to normal because less vesicles are able to be released.