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Ch. 14 The Autonomic Nervous System and Homeostasis
Amerman - Human Anatomy & Physiology 2nd Edition
Amerman2nd EditionHuman Anatomy & PhysiologyISBN: 9780136873822Not the one you use?Change textbook
All textbooksAmerman 2nd EditionCh. 14 The Autonomic Nervous System and HomeostasisProblem L3.B1
Chapter 14, Problem L3.B1

Many chemical warfare agents, such as the poisonous gas sarin, block the enzyme acetylcholinesterase in the synaptic cleft. What effects will this poison have on muscle contraction? What effects will it have on the autonomic nervous system? What symptoms would you expect to see from this poison?

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Understand the role of acetylcholinesterase: Acetylcholinesterase is an enzyme responsible for breaking down acetylcholine in the synaptic cleft. Acetylcholine is a neurotransmitter that stimulates muscle contraction and activates the autonomic nervous system. Blocking this enzyme leads to an accumulation of acetylcholine.
Analyze the effects on muscle contraction: Excess acetylcholine in the synaptic cleft causes continuous stimulation of muscle fibers. This results in prolonged muscle contraction, leading to spasms or tetany (sustained contraction).
Examine the effects on the autonomic nervous system: The autonomic nervous system relies on acetylcholine for signaling in both the parasympathetic and sympathetic divisions. Excess acetylcholine can overstimulate these systems, causing symptoms such as excessive salivation, sweating, and bronchoconstriction.
Identify expected symptoms: Symptoms of sarin poisoning include muscle spasms, difficulty breathing due to bronchoconstriction, excessive secretions (saliva, tears, mucus), constricted pupils, and potentially seizures. Severe cases can lead to respiratory failure and death.
Relate the physiological effects to treatment: Understanding the mechanism of sarin poisoning highlights the importance of treatments like atropine (which blocks acetylcholine receptors) and pralidoxime (which reactivates acetylcholinesterase) to counteract the effects of the poison.

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Key Concepts

Here are the essential concepts you must grasp in order to answer the question correctly.

Acetylcholinesterase Function

Acetylcholinesterase is an enzyme that breaks down the neurotransmitter acetylcholine in the synaptic cleft, which is crucial for muscle contraction and neurotransmission. By hydrolyzing acetylcholine, it prevents continuous stimulation of muscles and neurons. When inhibited by agents like sarin, acetylcholine accumulates, leading to prolonged muscle contraction and overstimulation of the nervous system.
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Muscle Contraction Mechanism

Muscle contraction is initiated when acetylcholine is released at the neuromuscular junction, binding to receptors on muscle fibers and triggering a series of events that lead to contraction. The influx of calcium ions into the muscle cells facilitates the interaction between actin and myosin filaments. Inhibition of acetylcholinesterase results in excessive acetylcholine, causing continuous stimulation and potentially leading to muscle fatigue or spasms.
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Autonomic Nervous System Effects

The autonomic nervous system (ANS) regulates involuntary bodily functions, including heart rate, digestion, and respiratory rate. Sarin's inhibition of acetylcholinesterase can lead to overstimulation of both the sympathetic and parasympathetic branches of the ANS, resulting in symptoms such as increased heart rate, excessive salivation, and respiratory distress. This dysregulation can cause severe physiological responses and potentially life-threatening conditions.
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Related Practice
Textbook Question

Which neurotransmitter(s) is/are used by sympathetic postganglionic neurons?


a. Epinephrine

b. Norepinephrine

c. Acetylcholine

d. Both a and b

e. All of the above

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Textbook Question

Which cranial nerves would be affected by a drug that stimulates the parasympathetic nervous system? Predict potential adverse effects that one might experience.

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Textbook Question

A patient, Dr. Young, has both asthma and high blood pressure. Her physician prescribed the drug propranolol to treat her hypertension; this drug blocks all types of β-adrenergic receptors. She also takes the drug albuterol for asthma, which activates β2 receptors on bronchial smooth muscle. Will the pairing of these two drugs cause problems for Dr. Young? Explain.

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Textbook Question

Differentiate between adrenergic and cholinergic receptors.

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Textbook Question

Explain what happens when sympathetic neurons stimulate the adrenal medulla. What purpose does this serve?

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Textbook Question

The poison curare (kyoo-RAH-ray) blocks the binding of acetylcholine to its receptors at the neuromuscular junction. What effects would you predict from such a poison? Can you think of any useful applications for it? Why might an overdose of it be lethal?

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