Step 1: Approach this from the immunology of the neuromuscular junction. Myasthenia gravis is an antibody-mediated disease, so identify the protein the autoantibodies attack. Step 2: The target is the nicotinic acetylcholine receptor on the muscle side of the synapse. Circulating anti-AChR antibodies reduce the number of functional receptors and flatten the post-synaptic folds, leaving transmission unable to keep up with repeated firing. Step 3: Clinically this explains the hallmark fatigability and the dramatic, if brief, improvement when an anticholinesterase floods the cleft with extra acetylcholine, partly overcoming the receptor shortage. Step 4: None of calcium, sodium or opioid receptors fits this autoimmune picture, so the blocked receptor is the acetylcholine receptor. \[\boxed{\text{Acetylcholine receptors}}\]