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?
Propose a targeted drug treatment for an individual with this disease that would help to improve the effects of the disease. Said in a different way, what is the mechanism that is failing in this disease, and what could be changed to bring it back to ânormalâ.
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?
Propose a targeted drug treatment for an individual with this disease that would help to improve the effects of the disease. Said in a different way, what is the mechanism that is failing in this disease, and what could be changed to bring it back to ânormalâ.
