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The nerve gas can be down-regulated first by up-regulating the response at the neuromuscular junction. Please explain exactly how this can be happen.

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Patrina Schowalter
Patrina SchowalterLv2
9 Aug 2019

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Myasthenia gravis is an autoimmune disease affecting the neuromuscular junction. In myasthenia gravis, weakness occurs when the nerve impulse to initiate or sustain movement does not adequately reach the muscle cells. This is due to an autoimmune response in which immune cells target and attack the body's own cells. Antibodies are produced that attach to "affected areas", preventing muscle cells from receiving chemical messages (neurotransmitters) from the nerve cell. Using your knowledge of muscle contraction and how the nerve stimulation reaches the muscle cell, explain this disorder and how it interferes with contraction. What specific part of the muscle might the "affected area" be? Explain your choice.Would the administration of ACH or acetylcholinesterase possibly help the symptoms of this disease? Explain which one you think would help and why.

1. As a Nursing student in Advanced Human Anatomy, you were ableto observe a total hip replacement. While the O.R. personnel whereprepping the patient for the surgical procedure, theanesthesiologist assumed (rightly so!) that you had some physiologybackground. As such, she launched into the following proceduralexplanation: The patient will need to be intubated, therefore hewill be given a single dose of the neuromuscular blocking agent,succinylcholine to provide muscular relaxation during the surgeryand to facilitate the insertion of the endotracheal tube. Theanesthesiologist asked you the following:


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A well-studied autoimmune and neuromuscular disease affects the neuromuscular junction of afflicted individuals. It turns out that antibodies attack the ligand receptor found on the skeletal muscle cells and reduces the number of these receptors, leading to weakness in eye muscles, facial muscles and in severe cases affects respiratory muscles.

The name and location of the receptor this disease attacks.

What neurotransmitter binds the affected receptors?

In comparing the monosynaptic pathway for an individual without the disease and with the disease, if the sensory neuron in both individuals received the same stimulus (both in intensity and frequency), would the relative amount of neurotransmitter released at the neuromuscular junction differ? Why or why not (meaning explain using the physiology)? (

Would the end plate potential (EPP) differ in a person without the disease versus someone with this disease? How, explain.]

Given the scenario, what branch of the nervous system does this disease affect, central or peripheral? Somatic, parasympathetic, or sympathetic?

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