You discover a mutant mouse whose skeletal muscles do not work properly. You remove a piece of muscle tissue in an attempt to discover the problem. The only abnormal thing you can find is that the acetylcholinesterase gene seems to be OVER-expressed, resulting in excess amount of this enzyme in and around the NMJ. How does this affect contraction?

You discover a mutant mouse whose skeletal muscles do not work properly. You remove a piece of muscle tissue in an attempt to discover the problem. The only abnormal thing you can find is that the acetylcholinesterase gene seems to be OVER-expressed, resulting in excess amount of this enzyme in and around the NMJ. How does this affect contraction?

Human Physiology: From Cells to Systems (MindTap Course List)

9th Edition

ISBN:9781285866932

Author:Lauralee Sherwood

Publisher:Lauralee Sherwood

Chapter8: Muscle Physiology

Section: Chapter Questions

Problem 11RE

See similar textbooks

Similar questions

Figure 38.37 Which of the following statements about muscle contraction is true? The power stroke occurs when ATP is hydrolyzed to ADP and phosphate. The power stroke occurs when ADP and phosphate dissociate from the myosin head. The power stroke occurs when ADP and phosphate dissociate from the actin active site. The power stroke occurs when Ca2+ binds the calcium head.
What would happen to muscle function if you ingested a toxin that completely inactivated troponin? The toxin inhibits its ability to change conformation. How would this affect muscle contraction?
What event causes a troponin-tropomyosin complex to regain its original shape in muscle relaxation? a. stimulation of ACh receptors b. diffusion of Na+ back into transverse tubules c. return of Ca2+ into the sarcoplasmic reticulum d. breaking of the bond with tropomyosin
If you introduced a chemical into a muscle fiber that blocked the voltage-gated calcium channels in the sarcoplasmic reticulum, what effect if any, would this have on the contraction of that muscle fiber?
The single-fiber twitch experiments shown here were generated by stimulating the muscle cell membranes to threshold with an electrode and measuring the resulting action potential and force. How would the results differ if Ca21 were removed from the extracellular solution just before the electrical stimulus was applied?
In the sliding filament theory of contraction, what prevents the filaments from sliding back to their original positions each time a myosin head releases to bind to next actin binding site?
Calmodulin is found in smooth muscle cells and performs a similar function to troponin in striated muscle fibers. However, calmodulin not only gets activated by Ca2+ but also slows the release of Ca2+ from the sarcoplasmic reticulum. How might this difference relate to the different kinds of contractions smooth muscles do in comparison to striated muscles?
In the process of muscle contraction, which of the following steps immediately precedes the sliding of tropomyosin causing exposure of actin? binding of acetylcholine to its receptor binding of calcium to troponin exocytosis of acetylcholine at NMJ binding of myosin head to actin's active site binding of ATP to the myosin head
If ligand-gated K+ channels were to open in an unstimulated muscle fiber,how would this affect the resting membrane potential?
How is a muscle cell excited and why does it lead to a contraction in the muscle?
Which of the following step(s) about the excitation of skeletal muscle is/are incorrect? 1. Acetylcholine is released and binds to motor end plate receptors 2. An action potential is created and moves down T-tubules 3. Calcium is released from the sarcoplasmic reticulum 4. Calcium ions bind to tropomyosin to shift troponin off the binding sites for cross-bridging 5. Myosin forms cross-bridges and binds with actin to pull it towards middle of sarcomere
In the process of muscle contraction, which of the following steps immediately comes after the propagation of an action potential down the t-tubules of a myofiber? sliding of tropomyosin causing exposure of actin binding of myosin head to actin's active site release of calcium from the terminal cisternae binding of acetylcholine to its receptor influx of sodium at the sarcolemma