Campbell Biology in Focus (2nd Edition)
2nd Edition
ISBN: 9780321962751
Author: Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, Jane B. Reece
Publisher: PEARSON
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Textbook Question
Chapter 37.4, Problem 2CC
Organophosphate pesticides work by inhibiting acetylcholinesterase, the enzyme that breaks down the neurotransmitter acetylcholine. Explain how these toxins would affect EPSPs produced by acetylcholine.
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The Structure of the acetylcholine receptor is shown below:
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Chapter 37 Solutions
Campbell Biology in Focus (2nd Edition)
Ch. 37.1 - Prob. 1CCCh. 37.1 - Describe the basic pathway of information flow...Ch. 37.1 - WHAT IF? How might increased branching of an axon...Ch. 37.2 - Under what circumstances could ions flow through...Ch. 37.2 - WHAT IF? Suppose a cells membrane potential shifts...Ch. 37.2 - Prob. 3CCCh. 37.3 - How do action potentials and graded potentials...Ch. 37.3 - In multiple sclerosis (from the Greek skleros,...Ch. 37.3 - Prob. 3CCCh. 37.3 - WHAT IF? Suppose a mutation caused gated sodium...
Ch. 37.4 - Prob. 1CCCh. 37.4 - Organophosphate pesticides work by inhibiting...Ch. 37.4 - MAKE CONNECTIONS Name one or more membrane...Ch. 37 - What happens when a resting neuron's membrane...Ch. 37 - Prob. 2TYUCh. 37 - Prob. 3TYUCh. 37 - Why are action potentials usually conducted in one...Ch. 37 - Which of the following is a direct result of...Ch. 37 - Suppose a particular neurotransmitter causes an...Ch. 37 - Prob. 7TYUCh. 37 - Prob. 8TYUCh. 37 - DRAW IT Suppose a researcher inserts a pair of...Ch. 37 - Prob. 10TYUCh. 37 - FOCUS ON EVOLUTION An action potential is an...Ch. 37 - Prob. 12TYUCh. 37 - SYNTHESIZE YOUR KNOWLEDGE The rattlesnake alerts...
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- After discussing his case with his physician, he learned that he had probably been the victim of pufferfish poisoning. The active toxin in the tissues of this fish is a chemical called tetrodotoxin (TTX). Tetrodotoxin is in a class of chemicals known as neurotoxins because it exerts its effects on neurons. The specific action of tetrodotoxin is that it blocks voltage-gated sodium ion channels. Define the following phrases and terms associated with the signs and symptoms of Dr. Westwood’s TTX poisoning: diaphoresis motor dysfunction paresthesias cyanotic hypoventilating bradycardia gastric lavage oxygen saturation As mentioned in the case description, tetrodotoxin is a molecule that blocks voltage-gated sodium ion channels. What is a voltage-gated sodium ion channel and what is its function? When nerve cells are at rest, there is an unequal amount of positive and negative charges on either side of a nerve cell membrane. This charge difference creates an electrical potential.…arrow_forwardThe Structure of the acetylcholine receptor is shown below: D. Briefly indicate what the role of the acetylcholine receptor is in an action potential.arrow_forwardAcetylcholine is a neurotransmitter that, when bound to its receptor, causes the receptor to open a channel that allows the flow of Na+ ions into neurons. When the Na+ ions begin to flow into the neuron, this change in the net charge across the neuronal cell membrane often triggers Ca2+ ion channels to open. In this scenario, the acetylcholine receptor would be acting as a channel, and the Ca2+ channels would be classified as voltage-gated; leaky ligand gated; voltage-gated symporter; antiporter None of the above. ionarrow_forward
- A patient has been exposed to the organophosphate pesticide malathion,which inactivates acetylcholinesterase. Which of the following symptoms would you predict: blurring of vision, excess tear formation, frequent or involuntary urination, pallor (pale skin), muscle twitching, orcramps? Would atropine be an effective drug to treat the symptoms?(See Clinical Impact 16.2 for the action of atropine.) Explain.arrow_forwardSarin is an inhibitor of acetylcholinesterase. Draw a mechanism that shows this.arrow_forwardThe graph shows a tracing of membrane potential change during the course of an action potential in a typical neuron. Predict the effect of exposure to the following neurotoxins. Briefly explain how you would expect the action potential to change in the presence of each toxin and why. A toxin produced by puffer fish which specifically binds to voltage-gated sodium channels and blocks the flow of sodium ions through the channel. A toxin found in scoprion venom which slows the closure of voltage-gated sodium channel inactivation gates. Assume that the cell is normally brought to threshold by an electrical stimulus applied to it, so that any change is due only to the presence of the toxin Precise values for voltage and duration are not important, just a general trend in how the action potential may differ from the typical trace shown is expected.arrow_forward
- The drug Buckeyium binds to the NMDA receptor at the orthosteric binding site (were glutamate would normally bind). Assume that glycine is already bound, and that magnesium is not blocking the NMDAR ion channel. If the channel does not open as a result of Buckeyium binding than Buckeyium would be considered aarrow_forwardBoth rhodopsin in vision and the muscarinic acetylcholine receptor in cardiac muscle are coupled to ion channels via G proteins. Describe the similarities and differences between these two systems.arrow_forwardWhen 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?arrow_forward
- Buckeyium is a medication that binds to the NMDA receptor at the orthosteric binding site (were glutamate would normally bind). Assume glycine is already bonded and magnesium isn't inhibiting the NMDAR ion channel. Buckeyium would be regarded a poison if the channel did not open as a consequence of its binding.arrow_forwardThe action potential generated in the squid giant axon requires voltage-gated potassium channels. Describe the shape of the action potential if these channels are blocked using TEA (Tetraethylammonium).arrow_forwardConotoxin is produced by marine cone snails. Among its effects is to block voltage-gated Ca2+ channels in n eurons. A. What anatomical part of a neuron would be affected by conotoxin? B. How would the neuron's action potential be affected by conotoxin? Explain, using at least TWO of the following terms: threshold, depolarization, repolarization, hyperpolarization, summation, IPSP, EPSP, exocytosis C. If conotoxin affected a somatic motor neuron, would this toxin cause muscle weakness or increased muscle tension? Explain why.arrow_forward
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