Questions: In the autoimmune disease myasthenia gravis (MG), the body makes self-reactive antibodies against the acetylcholine receptor on the postsynaptic cell, which block or destroy the receptor. A normally functional ACh receptor binds acetylcholine, opening an ion channel and producing an EPSP, but this doesn't happen in MG, which decreases the likelihood of the muscle fiber reaching threshold depolarization and contracting, causing muscle weakness. Additional considerations: Acetylcholinesterase is an extracellular enzyme that breaks down ACh to acetate and choline in order to terminate its effect. Not all nAChR's will be destroyed by the body's immune system. Which of the following treatments would produce additional muscle strength in a person with MG? treatment with an antibody to acetylcholine treatment with acetylcholinesterase treatment with an inhibitory neurotransmitter treatment with an acetylcholinesterase inhibitor treatment with a Na+/ K+ ATPase inhibitor

The answer is the fourth one: treatment with an acetylcholinesterase inhibitor.

Explanation for each option:

1. Treatment with an antibody to acetylcholine:

   • This would likely worsen the condition. Antibodies to acetylcholine would bind to acetylcholine, preventing it from interacting with any remaining functional acetylcholine receptors (AChRs). This would further reduce the likelihood of muscle contraction.

2. Treatment with acetylcholinesterase:

   • Acetylcholinesterase breaks down acetylcholine in the synaptic cleft. Increasing the amount of acetylcholinesterase would decrease the availability of acetylcholine, exacerbating muscle weakness in MG patients.

3. Treatment with an inhibitory neurotransmitter:

   • Inhibitory neurotransmitters generally reduce the likelihood of action potentials in neurons. This would not help in increasing muscle strength and could potentially worsen muscle weakness.

4. Treatment with an acetylcholinesterase inhibitor:

   • Acetylcholinesterase inhibitors prevent the breakdown of acetylcholine, increasing its concentration in the synaptic cleft. This would enhance the likelihood of acetylcholine binding to any remaining functional AChRs, thereby improving muscle contraction and strength in MG patients.

5. Treatment with a $\mathrm{Na}+/ \mathrm{K}+$ ATPase inhibitor:

   • Inhibiting the $\mathrm{Na}+/ \mathrm{K}+$ ATPase would disrupt the ionic gradients necessary for action potentials and muscle contractions. This would likely lead to further muscle weakness and other cellular dysfunctions.

Summary: The most effective treatment to produce additional muscle strength in a person with myasthenia gravis would be the use of an acetylcholinesterase inhibitor. This treatment increases the availability of acetylcholine in the synaptic cleft, thereby enhancing the chances of activating the remaining functional acetylcholine receptors and improving muscle contraction.