EBK BIOLOGY
11th Edition
ISBN: 8220102797352
Author: Raven
Publisher: YUZU
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Textbook Question
Chapter 46, Problem 3S
The nerve gas methylphosphonofluoridic acid (sarin) inhibits the enzyme acetylcholinesterase, required to break down acetylcholine. Based on this information, what are the likely effects of this nerve gas on muscle function?
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When the neurotransmitter acetylcholine (ACh) binds the acetylcholine receptor (a GPCR) on muscle cells, it causes them to contract. ZIGGY, a chemical analog of ACh, also binds to the same acetylcholine receptor on muscle cells, but instead causes the muscle cells to relax. For this reason, it is sometimes prescribed as a muscle relaxer. Explain in 3-4 sentences how ZIGGY could cause muscle relaxation.
How can both ZIGGY and ACh bind the same GPCR? And then how can they have different effects on the cells, despite binding to the same receptor on the same cells?
In light of the “all or none” law of muscle contraction, how can you explain twitch recruitment (also called the graded response) when stimulating the muscle versus stimulating the nerve? Explain the difference in stimulation voltage required to elicit a maximum response when stimulating the nerve versus the muscle directly?
Put these events that occur in skeletal muscle in the correct chronological sequence:
1. Activation of voltage-gated dihydropyridine (DHP) receptor in the T-tubule
2. Opening of mechanically-gated ryanodine receptors (RyR) on the sarcoplasmic reticulum
3. Na+ influx through ligand-gated ion channels on the motor end plate
4. Ca2+ binding to troponin
2, 1, 4, 3
4, 3, 2, 1
4, 3, 1, 2
3, 1, 4, 2
3, 1, 2, 4
Chapter 46 Solutions
EBK BIOLOGY
Ch. 46 - Exoskeletons and endoskeletons differ in that a....Ch. 46 - Worms use a hydrostatic skeleton to generate...Ch. 46 - Bone develops by one of two mechanisms depending...Ch. 46 - Which of the following statements best describes...Ch. 46 - Motor neurons stimulate muscle contraction via the...Ch. 46 - Prob. 6UCh. 46 - If you wanted to study the use of ATP during a...Ch. 46 - Place the following events in the correct order....Ch. 46 - You take X-rays of two individuals. Ray has been a...Ch. 46 - You have identified a calcium storage disease in...
Ch. 46 - How do the muscles move your hand through space?...Ch. 46 - How can osteocytes remain alive within bone? a....Ch. 46 - Swimming underwater using forelimbs for propulsion...Ch. 46 - If a drug inhibits the release of ACh, what will...Ch. 46 - Prob. 1SCh. 46 - Prob. 2SCh. 46 - The nerve gas methylphosphonofluoridic acid...Ch. 46 - If natural selection favors the evolution of wings...
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Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biology and related others by exploring similar questions and additional content below.Similar questions
- In the rare neuromuscular disorder Myasthenia Gravis, autoantibodies are produced which inhibit acetylcholine receptor (nicotinic receptor) activity. Explain how inhibition of acetylcholine receptor activity at the neuromuscular junction will affect the sequence of events in muscular excitation and contraction in response to stimuli, and muscle function? (Mention the effects on all the significant events involved in excitation and contraction of muscles, and how it would affect muscle function).arrow_forwardPut these events that occur in skeletal muscle in the correct chronological sequence: 1. Opening of mechanically-gated ryanodine receptors (RyR) on the sarcoplasmic reticulum 2. Ca²+ binding to troponin to initiate contraction 3. Activation of voltage-gated dihydropyridine (DHP) receptor in the T-tubule 4. Na+ influx through ligand-gated ion channels on the motor end plate 4, 3, 2, 1 2, 1, 4, 3 3, 1, 2, 4 4, 3, 1, 2 3, 1, 4, 2arrow_forwardIn the process called "excitation-contraction coupling" (the events that lead up to a muscle cell's contraction), what part of this process is disrupted by death? (Actually, all of it is disrupted by death, but we can pinpoint a linkage between death, and the onset of rigor mortis--as well as explaining why rigor mortis eventually ends.)arrow_forward
- 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 sarcomerearrow_forwardAcetylcholine is necessary for the depolarization of skeletal muscle cells. Which of the following statements concerning acetylcholine action is true. O acetylcholine is released in quanta from the sarcolemma membrane by exocytosis O acetylcholine is released in quanta from the postsynaptic membrane by exocytosis O acetylcholine enters the caveoli to depolarize the sarcolemma acetylcholine enters clathrin -coated vesiclec prior to its degradation by O acetylcholine attaches to transmitter-gated ion channels of the sarcolemma . During an action potential, depolarization occurs because: Channels for sodium ions in the cell membrane open and sodium flows into the cell O Both channels for sodium and potassium are closed O Channels for potassium ions in the cell membrane open and potassium leaves he cell Sodium potassium pump retums sodium to the outside of the cell and potassium to the inside Stroke occurs when a blood clot enters the cerebral ciruculatin, blocking an artery and causing…arrow_forwardWhy is it important to remove acetylcholine from its binding to acetylcholine receptors once the neural stimulus ends? What can be the possible consequence of the non-removal of acetylcholine to the skeletal muscle fiber?arrow_forward
- Succinylcholine act as adepolarising agent that prevents repolarization of the somatic motor neuron. Thus, no further ACh is released until drug is cleared. Name another site within the MNJ we could target to prevent muscle contraction, and explain why this would work.arrow_forwardFor the following five events, which is the correct sequence that describes the excitation and contraction of a skeletal muscle fiber? 1. Tropomyosin shifts, exposing the myosin-binding sites on actin. 2. Calcium is released from the sarcoplasmic reticulum and binds to the troponin complex. 3. An action potential is propagated down the transverse tubules. 4. Cycles of myosin cross-bridge formation and breakdown cause the thin filaments to slide toward the center of the sarcomere. 5. An action potential in a motor neuron causes the axon to release acetylcholine, which triggers an action potential in a muscle fiber. 1 → 2 → 3 → 4 → 5 3 → 2 → 4 → 1 → 5 2 → 1 → 3 → 5 → 4 5 → 3 → 2 → 1 → 4 4 → 3 → 1 → 2 → 5arrow_forwardWhen curare, a neuromuscular poison, is dropped onto an isolated muscle-nerve preparation in a laboratory, the muscle does not contract when the nerve is stimulated, even though neurotransmitter is released from the nerve cell. Why does this happen? How might this action of curare be lethal to an individual who has been poisoned?arrow_forward
- Acetylcholinesterase is the enzyme that breaks down and inactivates acetylcholine. Some nerve gases used as chemical weapons block acetylcholinesterase. What effect would such nerve gases have on muscle contraction?arrow_forwardWhether the statement, "Motor neurons trigger action potentials in muscle cell membranes that open voltage-sensitive Ca2+ channels in T tubules, allowing extracellular Ca2+ to enter the cytosol, bind to troponin C, and initiate rapid muscle contraction", is true or false.arrow_forwardDiscuss the similarities and differences by which Ca2+ activity is involved in initiating muscle contraction in skeletal versus smooth muscle fibers (hint: include Ca2+ sources, proteins it binds to, and signaling cascade it activates leading to contraction). (please explain in sentences, max 12 sentences)arrow_forward
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