In the disease myasthenia gravis, the human body makes-by mistake- antibodies to its own acetylcholine receptor molecules. These antibodies bind to and inactivate acetylcholine receptors on the plasma membrane of muscle cells. The disease leads to devastating progressive weakening of the muscles of people affected. Early on, they may have difficulty opening their eyelids, for example, and, in an animal model of the disease, rabbits have difficulty holding their ears up. As the disease progresses, most muscles weaken, and people with myasthenia gravis have difficulty speaking and swallowing. Eventually, impaired breathing can cause death. Explain which step of muscle function is affected

The nerve endings possess synaptic acetylcholine vesicles ready to be released. The action potential depolarizes the presynaptic terminal and increases the concentration of axoplasmic calcium; Acetylcholine molecules are thus released, so that the concentration of the neurotransmitter at postsynaptic (nicotinic) receptors is temporarily increased. This is followed by post-synaptic membrane depolarization, muscle membrane action potential with increased rnioplasmic calcium concentration, and finally muscle contraction. Acetylcholine is hydrolyzed by acetylcholinesterase and resynaptic at the presynaptic level by cholinecetyltransferase. The etiopathogenesis of myasthenia gravis is autoimmune and there are antibodies against acetylcholine receptors that circulate in the blood, as well as a decrease in the number of receptors on the motor plates, that is, it is produced by the postsynaptic blockage of the myoneural plaque, that generates fatigue and localized or generalized muscle weakness that is characterized by the worsening of the contractile force of the muscle.