BIOL350 CELL BIOLOGY TAKE-HOME 1 (100pts) Spring 2018 Name SFSUID 6. You are int

Question

BIOL350 CELL BIOLOGY TAKE-HOME 1 (100pts) Spring 2018 Name SFSUID 6. You are interested in creating drugs that affect nerve-muscle signaling. At first, you wish create an anesthetic that will prevent nerves from signaling to muscles to A. (e identity of one protein in thenurusclar kunction that can be targetod with your drug? B. (5pts) How can a drug affect the molecular function of the protein from Part A to lead to loss of nerve-muscle signaling? C. (5pts) After your success, you then wish to create a drug that prolongs muscle contraction. How can a drug affect the molecular function of the protein from Part A to lead to longer nerve- muscle signaling?

Explanation / Answer

For this exercise you have to bear in mind that it is a motor end plate.
A motor end plate is where an axon of a neuron and a muscle fiber "unite". As such there is no union, there is a small space where the synapse happens and where all the reactions happen which leads to an action potential and finally the contraction. The proteins that are in the membrane of the neuron (ie the presynaptic membrane) are several, but the most important are the voltage-dependent channels that allow calcium to pass through. In the membrane of the muscle fiber (or postsynaptic membrane) we also have several proteins involved, however one of the most important and studied are the acetylcholine receptors (or ligand-dependent channels) which once in contact with acetylcholine open and allow sodium ions to enter.

With this we can answer question 6A, the protein to be labeled will be the ligand-dependent channel (or acetylcholine receptor).

Now to answer question 6B, if an acetylcholine analog is synthesized that takes the place of the receptor without generating action potential, the acetylcholine will not be able to do its function and with this the channels will not be opened so that it will not enter the sodium to the cell and the potential for action will not be generated.

For 6C

There are already documented cases of this phenomenon, so that acetylcholine is not stuck in a prolonged way to the receptor there are acetylcholinesterase molecules in the synaptic space that break the acetylcholine molecules. Organphosphorus poisoning causes this by irreversibly inhibiting the function of acetylcholinesterase receptors remain open which causes seizures and other effects that can lead to death. For this case, it would be necessary to synthesize some molecule that is similar to organophosphorus that reversibly inhibits the enzyme.

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