Lab Report

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Lab Report Two Part One: Patient A is suffering from Clostridium botulinum because it prevents neurotransmitter release at the neuromuscular junction and causes flaccid paralysis. This is caused by no ACh in the cleft and no action potential in the muscle. There is no contraction of the muscles. Patient B is suffering from poison from the black widow. Calcium channels in the presynaptic terminal are opened so there will be ACh in the cleft, but it causes local paralysis so there will be no action potential in the muscles. Patient C is suffering from myasthenia gravis. If the patient has exertional fatigue and weakness that improves upon rest and returns back during activity then there would be no action potential in the neuron but there would be ACh in the cleft and an action potential in the muscles because the patient is able to contract and relax muscles. Part Two: It would do what ACh would do. When ACh binds with receptor cells it is initiating an action potential, if succinylcholine is an ACh agonist it should do the same. I do not think acetylcholinesterase on succinylcholine would have any effect other than normal blocking/uptake up the neurotransmitter because that is what acetylcholinesterase does. Part Three: I believe that these compounds are trying to make people feel better. These drugs are being used to treat depression. MAO inhibitor “makes you feel good.” It is an accumulation of norepinephrine in the cleft. SSRI’s increase serotonin by inhibiting its reuptake into the presynaptic

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