CAMPBELL BIOLOGY IN FOCUS (LL)-W/MOD.MA
3rd Edition
ISBN: 9780135686065
Author: Urry
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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Malathion is an insecticide commonly used in the horticultural industry. Many homeowners
apply this chemical to their trees to rid them of infestation by aphids or other
insects. Malathion is classified as an organophosphate insecticide. Exposure to malathion
is very dangerous to humans and animals because it acts as an irreversible inhibitor of
acetylcholinesterase. Predict what might happen to synaptic communication between
cholinergic neurons if an individual or animal was poisoned with malathion, and clearly describe the mechanisms at work.
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.…
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.
Chapter 37 Solutions
CAMPBELL BIOLOGY IN FOCUS (LL)-W/MOD.MA
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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- Sarin 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_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_forward
- Correct the following false statement: "Any cell that has the acetylcholine receptor will have the same response as any other cell that also has the acetylcholine receptor when exposed to acetylcholine". Explain why this statement is false.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_forwardBuckeyium 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_forward
- Vitamins B1, B6 and B12 are so-called "Neurotropic" vitamins. They may response to "Wallerian degeneration" in nerve system. Briefly describe"Wallerian degeneration" and how the "neurotropic" vitamins react with this process.arrow_forwardDepending on the size and complexity of the molecule, small chemical alterations can impart significant activity differences, especially if a certain part of the molecule is critical for binding. Considering this, select structure(s) below that are expected to have high cholinergic agonist activity based on what we leamed about acetylcholine's SAR.arrow_forwardDescribe the neurotransmitters shown in Section 11.14 in the selected neurotransmitters table. Give examples of how they might occur in the body.arrow_forward
- The neuotransmitter acetylcholine is released from presynaptic neurons in response to a nerve impulse and diffuses across the synaptic cleft or neuromuscular junction to a receptor on another neuron or a muscle cell. The nicotinic acetylcholine receptor is a pentamer containing four types of subunits, α2βγδ. Place the following in the correct order, from the release of acetylcholine from a neuron to receptor resensitization.arrow_forwardClostridium tetani toxin blocks the exocytosis of GABA. A. What anatomical part of a pre-synaptic neuron would be affected by this? B. How would a post-synaptic neuron’s likelihood of experiencing an action potential be affected by this toxin? C. Explain, using at least TWO of the following terms: threshold, depolarization, repolarization, hyperpolarization, summation, IPSP, EPSP, exocytosisarrow_forwardThe venom of many cobras contains a potent neurotoxin that binds to ligand-gated Na+ channels,causing them to open. Unlike ACh, which binds to and then rapidly unbinds from ligand-gated Na+ channels, the neurotoxin tends to remain bound to ligand-gated Na+ channels. How does this neurotoxin affect the nervous system’s ability to stimulate skeletal muscle contraction? How does it affect the ability of skeletal muscle fibers to respond to stimulation?arrow_forward
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