Table of contents

1. Introduction to Anatomy & Physiology5h 43m
2. Cell Chemistry & Cell Components12h 36m
3. Energy & Cell Processes10h 6m
4. Tissues & Histology10h 3m
5. Integumentary System2h 20m
6. Bones & Skeletal Tissue2h 16m
7. The Skeletal System2h 35m
8. Joints2h 17m
9. Muscle Tissue2h 33m
10. Muscles1h 11m
11. Nervous Tissue and Nervous System1h 35m
12. The Central Nervous System1h 6m
- Introduction to the Central Nervous System
  18m
- The Cerebrum
  48m
13. The Peripheral Nervous System1h 26m
14. The Autonomic Nervous System1h 38m
15. The Special Senses2h 41m
16. The Endocrine System2h 48m
17. The Blood3h 22m
18. The Heart3h 42m
19. The Blood Vessels3h 35m
20. The Lymphatic System3h 16m
21. The Immune System14h 37m
22. The Respiratory System3h 20m
23. The Digestive System2h 5m
24. Metabolism and Nutrition4h 0m
25. The Urinary System2h 39m
26. Fluid and Electrolyte Balance, Acid Base Balance37m
27. The Reproductive System2h 5m
28. Human Development1h 21m
29. Heredity3h 32m

14. The Autonomic Nervous System

Neurotransmitters of the ANS

Anatomy & Physiology

14. The Autonomic Nervous System

Neurotransmitters of the ANS

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3:27 minutes

Problem 7

Textbook Question

Inhibition of acetylcholinesterase by poisoning blocks neurotransmission at the neuromuscular junction because
a. ACh is no longer released by the presynaptic terminal.
b. ACh synthesis in the presynaptic terminal is blocked.
c. ACh is not degraded, so prolonged depolarization is enforced on the postsynaptic cell.
d. ACh is blocked from attaching to the postsynaptic ACh receptors.

Verified step by step guidance

Step 1: Understand the role of acetylcholinesterase (AChE). Acetylcholinesterase is an enzyme located in the synaptic cleft that breaks down acetylcholine (ACh) into acetate and choline after ACh has transmitted a signal across the synapse. This breakdown is essential for terminating the signal and allowing the postsynaptic cell to reset for the next signal.

Step 2: Analyze the effect of AChE inhibition. If acetylcholinesterase is inhibited, ACh will not be degraded in the synaptic cleft. This means that ACh will continue to bind to the postsynaptic acetylcholine receptors, causing prolonged stimulation of the postsynaptic cell.

Step 3: Consider the consequences of prolonged ACh activity. Prolonged binding of ACh to its receptors on the postsynaptic cell leads to continuous depolarization of the postsynaptic membrane. This sustained depolarization prevents the cell from resetting and responding to new signals, effectively blocking neurotransmission at the neuromuscular junction.

Step 4: Evaluate the incorrect options. Option (a) is incorrect because ACh is still released by the presynaptic terminal. Option (b) is incorrect because ACh synthesis is not affected by AChE inhibition. Option (d) is incorrect because ACh is not blocked from attaching to the receptors; rather, it continues to bind excessively due to lack of degradation.

Step 5: Identify the correct answer. Based on the analysis, the correct answer is (c): 'ACh is not degraded, so prolonged depolarization is enforced on the postsynaptic cell.' This explains how inhibition of acetylcholinesterase disrupts neurotransmission at the neuromuscular junction.

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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 acetylcholine (ACh) in the synaptic cleft after it has been released from the presynaptic terminal. This degradation is crucial for terminating the signal between neurons and muscle cells, allowing for proper muscle relaxation and preventing continuous stimulation.

Neuromuscular Junction

The neuromuscular junction is the synapse or connection point between a motor neuron and a muscle fiber. It is where the neurotransmitter acetylcholine is released to stimulate muscle contraction. Proper functioning of this junction is essential for voluntary movement and muscle control.

Prolonged Depolarization

Prolonged depolarization occurs when acetylcholine remains in the synaptic cleft due to the inhibition of acetylcholinesterase. This leads to continuous stimulation of the postsynaptic muscle cell, preventing it from returning to its resting state, which can result in muscle fatigue or paralysis.

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