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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Problem L2.3

Textbook Question

The drug neostigmine blocks the activity of the enzyme acetylcholinesterase in the synaptic cleft. Predict the effects of this drug.

Verified step by step guidance

Understand the role of acetylcholinesterase: Acetylcholinesterase is an enzyme located in the synaptic cleft that breaks down the neurotransmitter acetylcholine into acetate and choline, terminating its action at the synapse.

Recognize the effect of blocking acetylcholinesterase: If neostigmine inhibits acetylcholinesterase, acetylcholine will not be broken down as efficiently, leading to an accumulation of acetylcholine in the synaptic cleft.

Predict the physiological outcome: The increased concentration of acetylcholine will result in prolonged stimulation of acetylcholine receptors on the postsynaptic membrane, enhancing cholinergic signaling.

Consider the potential effects on the body: Prolonged stimulation of acetylcholine receptors can lead to increased muscle contraction, improved transmission at neuromuscular junctions, and potentially overstimulation of parasympathetic nervous system functions (e.g., increased salivation, slowed heart rate).

Relate to clinical applications: Neostigmine is often used to treat conditions like myasthenia gravis, where it helps improve muscle strength by enhancing neuromuscular transmission, or to reverse the effects of muscle relaxants used during surgery.

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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 the space between nerve cells. By hydrolyzing acetylcholine, it terminates the signal transmission between neurons and muscle cells, allowing for muscle relaxation and preventing continuous stimulation.

Neostigmine Mechanism of Action

Neostigmine is a reversible inhibitor of acetylcholinesterase, meaning it binds to the enzyme and prevents it from breaking down acetylcholine. This leads to an accumulation of acetylcholine in the synaptic cleft, resulting in prolonged stimulation of the postsynaptic receptors, which can enhance muscle contraction and improve neuromuscular transmission.

Clinical Implications of Neostigmine

Neostigmine is commonly used in the treatment of myasthenia gravis, a condition characterized by weakness in the skeletal muscles. By increasing acetylcholine levels, neostigmine helps improve muscle strength and function. However, excessive inhibition of acetylcholinesterase can lead to cholinergic crisis, characterized by muscle twitching, respiratory distress, and other symptoms due to overstimulation of the neuromuscular junction.

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Neuropeptides that act as natural opiates include

a. Substance P

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c. Tachykinins

d. Enkephalins

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Receptors that bind acetylcholine at the postsynaptic membrane are:

(a) Chemically gated channels

(b) Voltage-gated channels

(d) Mechanically gated channels

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Since at any moment a neuron is likely to have thousands of neurons releasing neurotransmitters at its surface, how is neuronal activity (to fire or not to fire) determined?

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In the Netherlands a young man named Jan was admitted to the emergency room. He and his friends had been to a rave. His friends say he started twitching and having muscle spasms which progressed until he was 'stiff as a board.' On examination, staff found a marked increase in muscle tone and hyperreflexia involving facial and limb muscles. In his pocket, he had unmarked dark yellow tablets with dark flecks. Analysis of the tablets showed them to contain a mixture of ecstasy and strychnine. Ecstasy would not cause this clinical picture, but strychnine, which blocks glycine receptors, could. Explain how.

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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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Textbook Question

Match the following neurotransmitters with their correct description.

_____ GABA

_____ Dopamine

_____ Substance P

_____ Acetylcholine

_____ Glutamate

_____ Endorphins

_____ Norepinephrine

a. Neuropeptide involved in transmission of pain

b. Neurotransmitter released at the neuromuscular junction

c. Major excitatory neurotransmitter in the brain

d. Major inhibitory neurotransmitter in the brain

e. Neuropeptide involved in relief of pain

f. Catecholamine involved in the autonomic nervous system

g. Catecholamine involved in movement and behavior

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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

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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