The muscle weakness of myasthenia gravis results from loss of acetylcholine receptors in the end-plate membrane. the motor neuron action potential being too small to shock the muscle fibers. insufficient acetylcholine release from presynaptic vesicles. excessive acetylcholinesterase that destroys the neurotransmitter. All of the answers probably contribute to the muscle weakness.

The correct answer is ''loss of acetylcholine receptors in the end-plate membrane.''

Explanation:

Myasthenia gravis represents a human autoimmune disease. The neuromuscular junction abnormalities that occur in this disease are due to antibody-mediated processes. A reduction in the number of functional acetylcholine receptors on the postsynaptic membrane was established to contribute to the physiological abnormalities of myasthenia gravis. The reduction in receptors is due to immunological alterations directed against the acetylcholine receptor. Normally, when acetylcholine binds to its receptor, it opens allowing the rapid entry of cations, especially sodium. With this, the depolarization of the postsynaptic region of the muscle fiber occurs. Although acetylcholine is normally released in myasthenia gravis, it is not capable of causing an action potential in the muscle sufficient to initiate or weaken contraction. In patients with myasthenia gravis, failure to activate muscles is responsible for myasthenic fatigue. Most patients have elevated serum titers of antireceptor antibodies, which in turn accelerate receptor degradation.