KINS 1100 Lecture Notes - Lecture 7: Troponin

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oliveferret431

9 Jan 2019

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Electrical excitability : ability to receive and respond to stimuli, conduct electrical impulses. Extensibility : ability to be stretched or extended w/out damaging the tissue. Elasticity : ability to return to original resting length after contraction or extension. Skeletal muscle fascicle muscle fibers myofibrils. Sarcoplasmic reticulum : modified smooth er, contains calcium ions. Transverse tubule : extension of sarcolemma, runs along transverse plane. Sarcomere : smallest contractile unit of muscle, repeating pattern. Thick filament (myosin) : contain myosin (rod-like tail and 2 heads) Atpase (breaks down atp and releases energy to start muscle contraction) Thin filament (actin) : a helical polymer of globular subunits called actin. Myosin-binding sites are located on dark area of actin. Don"t lose their lengths, but the sarcomere shortens when muscles contract. Components: -axon terminal/synaptic end bulb of presynaptic neuron. Brain motor command neuromuscular junc. excitation-contraction coupling release of calcium. Action potential occurs when na + are released into the motor end plate.

Related Questions

12.

Explain what happens to microfilaments within cells treated with cytochalasin D and why existing actin polymers eventually depolymerize. Fill in the blanks in the explanation below using words from the selections below.

Cytochalsin D _______ of monomers at ______ of existing filaments. When the concentration of G-actin in the cytosol is _______ the critical concentration, the loss of monomers at __________ of existing filaments eventually results in their shortening.

** Selections: prevents addition; equal to; plus ends; facilitates loss; above; below; both minus and plus ends; minus ends

18.

What effect does VX, a typical but potent acetylcholinesterase inhibitor, have on muscle function? Fill in the blanks in the explanation below. A word bank of choices follows.

Because the removal of acetylcholine is inhibited, the muscle membrane at the nueromuscular junction will remain _____ for an abnormally long period, causing the muscles to remain in a ______ state. The prolonged ______ in turn would be propagated via the T tubule system to ________ . The result would be prolonged release of calcium, resulting in sarcomere _______ via the effects of calcium on ________.

***Selections: polarized; depolarized; polarization; depolarization; shortening; relaxing; contracted; the sarcoplasmic reticulum; the troponin system; myosin; Z lines

1)Describe the directions in which the two motor proteins, kinesin and dynein, travel along a microtubule. Which of the two proteins moves materials towards the Golgi and which moves materials away from the Golgi? Lastly, what is the speed of kinesin dependent on?

2)What are microfilaments crucial for? How do they self-assemble? Which end do they prefer to elongate from?

3)Describe what types of filaments are in each of the bands of the sarcomere. As a muscle fiber is shortened, describe what happens to each of the bands in the sarcomere as the Z lines move inwards.

4)Describe the role of calcium ions in muscle contraction.

5)List the various types of actin-binding proteins

6) A. What are 3 functions of the cytoskeleton?

B.What are the three filaments that compose the cytoskeleton, and what are they composed?

7)How do they see the internal structures of cells in the microscope? What do proteins get labeled with?

8)Myosin II action (Figure 9.61) differs from that of kinesin (Figure 9.15) in that one of the kinesin heads is always in contact with a microtubule, whereas both myosin heads become completely detached from the actin filament. How are these differences correlated with the two types of motor activities in which these proteins engage?

9)If a myofibril were pulled so that the sarcomeres increased in length by approximately 50 percent, what effect would you expect this to have on the contractile ability of the myofibril? Why? What effects would this have on the H, A, and I bands?

10)Because cytoplasmic vesicles are seen to move in both directions within an axon, can you conclude that some microtubules are oriented with their plus end facing the axon terminus and others oriented with the opposite polarity? Why or why not?

Question 5. Dr. Campbell used an elliptical trainer for 40 minutes at the gym. Although the workload remained constant, Dr. Campbellâs heart-rate rose to 150 beats per minute during the first 5 minutes, stayed at that level for the next 25 minutes and then started to rise. It was 180 beats per minute at the end of the exercise period.

What was the time interval between QRS complexes when Dr. Campbellâs heart rate was 180 beats per minute?

a. 3.3 ms

b. 33 ms

c. 333 ms

d. 3333 ms

Question 6. In the question 5 above, Dr. Campbellâs heart rate is most likely to have risen during the last 10 minutes of exercise because his:

a. lungs were becoming congested

b. atrial cells were fatigued

c. extracellular Ca2+ concentration had increased

d. hematocrit increased due to sweating

Question 7. A Physiology student is sitting still in a cold igloo. After 30 minutes, she stands up, walks slowly around the igloo, and suddenly starts to shiver.

The student preserved their core temperature while they were sitting by:

a. depressing their Frank-Starling mechanism

b. decreasing the extracellular Ca2+ concentration

c. relaxing smooth muscles in their peripheral circulation

d. increasing the resistance of arterioles in their arms and legs

Question 8. In the question 7 above, the student started to shiver soon after walking because:

a. their atria started to fibrillate

b. their ventricles started to fibrillate

c. blood moved to the periphery, became cold, and chilled the core when it returned to the chest

d. the ATP concentration in their skeletal muscles had dropped to zero

Please use the following scenario for answering the questions 9 and 10.

A newly discovered drug binds to myosin molecules in cardiac muscle (and nowhere else) and increases the probability that myosin molecules in ventricular cells will bind to actin filaments when the intracellular Ca2+ concentration rises. The drug is being tested as a potential therapy for patients with heart failure.

Question 9. This drug might help people who have low cardiac output by:

a. increasing peripheral resistance

b. increasing the force developed by ventricular cells

c. increasing the isovolumic contraction time

d. increasing heart rate

Question 10. The increased binding of cardiac myosin molecules to actin might prevent the drug from being a useful treatment by:

a. slowing ventricular relaxation

b. decreasing the duration of systole

c. decreasing resistance of capillaries

d. slowing heart rate

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KINS 1100 Lecture Notes - Lecture 7: Troponin

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