1. (B) Levels of ACh at the muscle end-plates
2. (A) Autoimmune response
3. (E) Neostigmine
1.B) Myasthenia gravis is an autoimmune disease in which antibodies damage postsynaptic nicotinic acetylcholine receptors. This damage prevents the firing of an action potential in the postsynaptic membrane. Tensilon is a readily reversible acetylcholinesterase inhibitor that increases acetylcholine levels in the neuromuscular junction, thereby increasing the strength of muscle contraction.
2.A) Myasthenia gravis is an autoimmune disease characterized by the presence of anti–acetylcholine receptor antibodies in the plasma. Overexertion can cause junction fatigue, and both a decrease in the density of voltage-sensitive Ca++ channels in the presynaptic membrane and botulinum toxicity can cause muscle weakness. However, these effects are presynaptic and therefore would not be reversed by acetylcholinesterase inhibition. Although the macro-motor units formed during reinnervation following poliomyelitis compromise the patient’s fine motor control, they do not affect muscle strength.
3.E) Neostigmine is an acetylcholinesterase inhibitor. Administration of this drug would increase the amount of acetylcholine (ACh) present in the synapse and its ability to sufficiently depolarize the postsynaptic membrane and trigger an action potential. Botulinum toxin antiserum is effective only against botulinum toxicity. Curare blocks the nicotinic ACh receptor and causes muscle weakness. Atropine is a muscarinic ACh receptor antagonist, and halothane is an anesthetic gas. Neither atropine nor halothane has any effect on the neuromuscular junction.