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IB 132 Spring 2019

Name____ _____________

Homework 1 Section____ _______________ Instructions: Type in your name and section number (above) and answers to the following questions, save it as a new file with your first initial, last name, HW1. For example EVanHalenHW1. Upload the file to this assignment tab prior to the due date. Part 1: Review Questions (8 points) 1. Label the following EEG waves (alpha, beta, delta, theta). When do they occur? (1 point each) This is theta EEG wave, which occurs in NREM sleep, mainly dominating the N1 stage.

This is delta EEG wave, which occurs in stage N3 of NREM sleep.

This is beta EEG wave, which occurs in the time of alert wakefulness. It is also similar to REM pattern. This is alpha EEG wave, which occurs in the time of relaxed wakefulness and relaxed drowsiness, and stage N1 of NREM sleep.

Compare brain activity in REM versus NREM sleep. During REM sleep, a person’s EEG shows intense activity that is similar to the beta waves during alert and awake state. Also, brain oxygen consumption is higher during REM sleep than during the NREM or awake states. For the three states in NREM sleep, the frequency of brain waves gets lower and has larger amplitude as it moves from N1 to N2 to N3. In N1 Sleep, the dominant wave is the theta pattern. Then in N2 sleep, the theta rhythm is interrupted by sleep spindles and largeamplitude K complexes. In N3 sleep, delta waves start to appear together with theta rhythm, but the dominant pattern becomes a delta rhythm as N3 stage continues.

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2. Describe the crossbridge cycle as it relates to muscle contraction by answering the following:

a. Put the images (above) in the correct order starting with image A. (1 point) ABDCE b. What is the purpose of tropomyosin and how is it affected by calcium? (1point) Tropomyosin partially covers the myosin-binding site on each action molecule, so to prevent the cross-bridge from making contact with the actin. When calcium is present and binds to troponin, the shape of troponin changes and allows tropomyosin to move away from the blocking site, which allows cross-bridge formation. When calcium is removed from the troponin, the tropomyosin return to its blocking site, then the cross-bridge cycle stops, and the muscle fiber relaxes. c. Rigor mortis is when the body becomes very stiff right after death. Rigor mortis can last for several hours, after which the dead body becomes limp. This process has something to do with the crossbridge cycle. Explain what causes rigor mortis. (2 points) When a person is dead, he cannot form new ATP anymore, so the ATP concentration in his body drops. Without ATP, there is no allosteric modulator to weaken the binding of myosin to actin, so the muscle remain bounded to each other, producing a rigid condition which thick and thin filaments cannot slide away from each other. Part 2: Case Studies (12 points) Case Study 1: Jennifer Slater is a biochemist working for a bioweapons lab at the CDC. She is currently working on a project to develop a new neurotoxin and is using sarin as a model substance. While working one day, the lab alarms go off and Jennifer accidentally knocks a vial of sarin over and a bit of the liquid splashes onto her arm between her gloves and lab coat. She suddenly starts to feel dizzy, her heart starts pounding harder than ever, and she has shortness of breath. She feels incredibly sluggish and tries to get to the exit. As she approaches the lab door, her muscles cramp up and she falls down and hits her head, knocking her unconscious. Her colleague from across the hall happens to see her fall and calls for help. Jennifer is given oxygen and taken to the nearby hospital, which happens to have a neuromuscular specialist. Jennifer is admitted to the hospital and Dr. Wayne examines her. Jennifer is unconscious but seems to be experiencing some paralysis, so Dr. Wayne orders blood work. Results are listed below.

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a) Which of Jennifer’s levels are abnormal? (1 point each) Her AChE activity is lower than the normal range. b) What is the role of acetylcholinesterase (AChE) in the neuromuscular junction? AChE is an enzyme that can degrade acetylcholine in the neuromuscular junction so to stop the excitatory effects on the postsynaptic neuron. Hence, AChE ensure that the postsynaptic neuron would not be excited for a long time which may lead to paralysis or death because the muscles cannot relax. c) What is the mechanism of action of sarin or a sarin-like chemical? Just like ACh, Sarin and a sarin-like chemical can also bind to the active site of AChE, which then inhibit AChE, so that it cannot bind to ACh anymore and cannot degrade ACh. Then there will be excess ACh accumulating in the neuromuscular junction and the postsynaptic neurons would be excited for a long time which may lead to paralysis or death. d) How would exposure to a sarin-like poison affect the amounts of Na+ going into the muscle cell? Explain all the steps. When a person is exposed to sarin-like poison, his ACh in his neuromuscular junction cannot be degraded since most of the AChE was inactivated by the poison. Then the ACh, which is accumulated in the junction, will binds to its receptor due to constant stimulation and there will be an increase in membrane’s permeability to Na+ since the Na+ channels are opened. Gradually, as more and more Na+ moves into the cells, the cell membrane depolarized. e) How would exposure to sarin affect Ca+2 levels inside the sarcoplasmic reticulum and cytoplasm? Explain. When the membrane is depolarized and reached its threshold, action potential is fired continuously. During the firing of action potential, the depolarization propagated along the Ttubules. Then the Calcium channels open in the terminal cisternae of the sarcoplasmic reticulum, which allows the release of Ca2+. As a result, the Ca2+ level in sarcoplasmic reticulum will decreased and the Ca2+ level in the cytoplasm will increased.

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f) How do these altered Ca+2 levels affect the position of the actin and myosin filaments? Explain how this leads to Jennifer’s major symptom. Ca2+ is used to bind to troponin and cause tropomyosin to unblock the binding site, which allows formation of cross-bridges. In Jennifer’s case, her Ca2+ level in the cytoplasm is very high causing actin filaments and myosin filaments to stay connected due to overstimulation, so her muscles cramp up and becomes tighten. With a high Ca2+ level in cytoplasm, Jennifer cannot relax her muscles. Case Study 2: A 25-year-old preschool teacher, Sandy Thompson, has not been feeling like herself lately. She has been feeling quite tired and her co-workers have commented on her droopy eyelids. Additionally, she is experiencing weakness in her arms and legs, has difficulty talking clearly and even her students’ parents have been concerned that Sandy hasn’t been looking very happy at work. One day at lunch, Sandy started to choke on her food, causing one of her coworkers to perform the Heimlich maneuver on her. While the scare didn’t cause any permanent damage, Sandy is convinced that it is time to go see a doctor. When she finally arrives at her appointment with Dr. Wayne, she explains to Dr. Wayne what has been going on, and the doctor decides to run a few blood tests. Sandy’s blood work results are presented below.

a) Summarize the symptoms that Sandy is experiencing. They are all related to one underlying problem. (1 point each) She is experiencing tiredness, droopy eyelids, weakness in arms and legs, has difficulty talking clearly, and chokes on her food. b) What levels from her blood work are abnormal? Her blood has antibodies for ACh Receptors. c) How would antibodies against ACh receptors affect the neuromuscular junction and the influx of Na+ into the cell? Antibodies against ACh receptors will bind to the ACh receptors and inactivate them, so that ACh cannot bind to its receptors and will be accumulated in the neuromuscular junction. Since ACh receptors are inhibited by the antibodies, the permeability of Na+ permeability will decrease, so there will not be any influx of Na+ and the cell would not be able to depolarize. 4

d) How would antibodies against the ACh receptors affect the levels of Ca+2 inside the sarcoplasmic reticulum? Explain. Antibodies receptors inhibited the ACh receptors, so the permeability of Na+ permeability will decrease and the influx of Na+ will decrease. Without depolarization by the influx of Na+, there will not be any firing of action potential. Without action potential, the DHP receptors will not induce the open of ryanodine receptor channels, so there will be no release of Ca2+ from sarcoplasmic reticulum and the sarcoplasmic reticulum maintains high storage (or an increase) of Ca2+. e) Explain the effect this has on the actin and myosin filaments. Explain how this leads to Sandy’s symptoms. Ca2+ is used to bind to troponin and cause tropomyosin to unblock the binding site, which allows formation of cross-bridges. In Sandy’s case, her Ca2+ level in the cytoplasm is very low, which causes the blocking action of tropomyosin, so there is little/no sliding movement between actin filament and myosin filament because actin cannot bind to myosin. With a low Ca2+ level in cytoplasm, Sandy cannot have enough muscle contraction to perform daily activity, so she will feel weak in arms and legs, has droopy eyes, and has difficulty in talking and eating. f) What disorder does Sandy have? How do we treat/manage this diagnosis? [Look it up if you are not sure] Sandy has Myasthenia gravis. We can give Sandy pyridostigmine that increases the amount of acetylcholine available to stimulate the receptors, Anti-acetylcholinesterase agents that allow acetylcholine to remain at the neuromuscular junction longer, Corticosteroids that suppress the abnormal action of the immune system that occurs in MG, surgical removal of thymus can also suppress the abnormal action of the immune system.

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