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Ch. 11 Fundamentals of the Nervous System and Nervous Tissue
Marieb - Human Anatomy & Physiology 11th Edition
Marieb, Hoehn11th EditionHuman Anatomy & PhysiologyISBN: 9780136874034Not the one you use?Change textbook
Chapter 11, Problem 23

When admitted to the emergency room, Sean was holding his right hand, which had a deep puncture hole in its palm. He explained that he had fallen on a nail while exploring a barn. Sean was given an antitetanus shot to prevent neural complications. Tetanus bacteria fester in deep, dark wounds, but how do their toxins travel in neural tissue?

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1
Understand that tetanus bacteria produce a toxin called tetanospasmin, which affects the nervous system by interfering with neurotransmitter release.
Recognize that the toxin does not travel freely in the bloodstream but instead moves within the nervous system by retrograde axonal transport.
Recall that retrograde axonal transport is a process where substances are carried from the nerve endings back toward the cell body along the axon, using motor proteins like dynein.
Apply this knowledge to the scenario: the tetanus toxin enters peripheral motor neurons at the wound site and travels backward along the axon to the central nervous system (spinal cord and brainstem).
Conclude that this mode of transport allows the toxin to reach inhibitory interneurons in the CNS, leading to the characteristic muscle spasms and rigidity seen in tetanus.

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Key Concepts

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

Tetanus Bacteria and Toxin Production

Clostridium tetani bacteria thrive in deep, anaerobic wounds like punctures. They produce tetanospasmin, a potent neurotoxin responsible for the symptoms of tetanus. Understanding the bacteria's environment and toxin production is key to grasping the infection's progression.
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Neural Pathways for Toxin Transport

Tetanospasmin travels from the wound site to the central nervous system by binding to peripheral nerve terminals. It moves retrogradely along motor neurons via axonal transport, bypassing the bloodstream, to reach inhibitory interneurons in the spinal cord and brainstem.
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Mechanism of Tetanus Neurotoxicity

Once in the central nervous system, tetanospasmin blocks the release of inhibitory neurotransmitters like GABA and glycine. This leads to uncontrolled muscle contractions and spasms characteristic of tetanus. The toxin’s neural transport and action explain the clinical symptoms.
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Textbook Question

Local anesthetics block voltage-gated Na⁺ channels. General anesthetics are thought to activate chemically gated Cl⁻ channels, thereby rendering the nervous system quiescent while surgery is performed. What specific process do anesthetics impair, and how does this interfere with nerve impulse transmission?

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Rochelle developed multiple sclerosis when she was 27. After eight years she had lost a good portion of her ability to control her skeletal muscles. How did this happen?

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Textbook Question

The effects of neurotransmitter binding are very brief. Explain.

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Textbook Question

a. Contrast unipolar, bipolar, and multipolar neurons structurally.

b. Indicate where each is most likely to be found.

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Textbook Question

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

What is the polarized membrane state? How is it maintained? (Note the relative roles of both passive and active mechanisms.)

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