The neuronal disorder myasthenia gravis is characterized by muscle weakness. The pathophysiologic features of myasthenia result from a shortage of nicotinic receptors on the motor end plate. Myasthenia patients have antibodies in their plasma that bind the nicotinic receptors and so block these receptors for acetylcholine binding. This results in a decreased sodium influx and thus the failure in muscle contraction.
Moreover, because the acetylcholine can not bind the receptor, more acetylcholine is available for conversion by the cholinesterase enzymes. Treatment of myasthenia gravis involves suppression of the immune response and increase of the acetylcholine concentration in the synaptic cleft (by decreasing the activity of the cholinesterases).
In myasthenia gravis, muscle contraction can NOT be sustained because the number of transmitter-receptor interaction is too low.
Extra info: Myasthenia gravis is due to a deficit of nicotinic receptors on the end plate. The low number of transmitter-receptor interactions can not generate enough action potentials in the muscel cell.