Step 1: Frame the problem at the neuromuscular junction. Normal transmission needs acetylcholine released from the nerve to bind nicotinic receptors on the muscle end plate. An autoimmune attack on those receptors will impair this step.
Step 2: In myasthenia gravis, circulating IgG antibodies bind and deplete the postsynaptic nicotinic acetylcholine receptors and damage the junctional folds. The end plate potential then fails to reach threshold, especially on repeated activity, giving the hallmark fatigable weakness. Therefore the acetylcholine receptors are the blocked receptors.
Step 3: Exclude the others. Antibodies to presynaptic calcium channels belong to Lambert-Eaton syndrome (often paraneoplastic). Sodium-channel and opioid-receptor pathology do not cause this disorder. The diagnostic improvement with anticholinesterase drugs (more acetylcholine competing for the few remaining receptors) confirms the receptor involved.
\[\boxed{\text{Acetylcholine receptors}}\]