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Chapter Summary

This chapter discusses the structure and function of neurons, including the components of the neuron and the mechanisms of action potential generation. It explains the effects of potassium levels on neuronal excitability, the role of myelin in nerve conduction, and the classification of nerve fibers. Additionally, it covers the types of glial cells and their functions, as well as the impact of demyelinating diseases on nerve conduction.
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0% found this document useful (0 votes)
3 views1 page

Chapter Summary

This chapter discusses the structure and function of neurons, including the components of the neuron and the mechanisms of action potential generation. It explains the effects of potassium levels on neuronal excitability, the role of myelin in nerve conduction, and the classification of nerve fibers. Additionally, it covers the types of glial cells and their functions, as well as the impact of demyelinating diseases on nerve conduction.
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

International Medical University

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Ganong's Review of Medical Physiology, 26e

Chapter 4: Excitable Tissue: Nerve

CHAPTER SUMMARY
Neurons are composed of a cell body (soma) that is the metabolic center of the neuron, dendrites that extend arborize extensively and are a
common zone for receiving input to the neuron, the initial segment of the axon where the action potential is initiated, and a long axon that
conducts the action potentials.

The resting membrane potential of neurons is about –70 mV, which is close to the equilibrium potential for K+. During hyperkalemia, the resting
potential moves closer to the threshold for eliciting an action potential, thus the neuron becomes more excitable. During hypokalemia, the resting
membrane potential is reduced and the neuron is hyperpolarized.

In response to a depolarizing stimulus, voltage­gated Na+ channels are activated; when the threshold potential is reached, an action potential
results. The membrane potential moves toward the equilibrium potential for Na+. The Na+ channels are rapidly inactivated before returning to the
resting state.

The direction of the electrical gradient for Na+ is reversed during the overshoot because the membrane potential is reversed; this limits Na+ influx.
Voltage­gated K+ channels open to complete the process of repolarization. The slow return of the K+ channels to the closed state explains after­
hyperpolarization, followed by a return to the resting membrane potential.

The axons of many neurons are wrapped in myelin, a protein­lipid complex that is an effective insulator; depolarization of myelinated axons
travels from one node of Ranvier to the next, with the current sink at the active node serving to electrotonically depolarize to the firing level the
node ahead of the action potential.

Nerve fibers are divided into different categories (A, B, and C) based on axonal diameter, conduction velocity, and function. A numerical
classification (Ia, Ib, II, III, and IV) is also used for sensory afferent fibers. These various classes differ in their sensitivity to hypoxia and anesthetics.

Orthograde transport occurs along microtubules that run the length of the axon and requires two molecular motors: dynein and kinesin. It moves
from the cell body toward the axon terminals and has both fast (400 mm/day) and slow (0.5–10 mm/day) components. Retrograde transport goes
in the opposite direction (from nerve ending to cell body) at a rate of about 200 mm/day.

There are two main types of glia: microglia and macroglia. Microglia are scavenger cells. Macroglia include oligodendrocytes, Schwann cells, and
astrocytes. Oligodendrocytes and Schwann cells are involved in myelin formation; astrocytes produce substances that are tropic to neurons and
help maintain the appropriate concentration of ions and neurotransmitters.

Patchy destruction of myelin within the CNS associated with multiple sclerosis delays the conduction in axons. Autoimmune reactions to the
myelin proteins P0 and PMP22 cause Guillain–Barré syndrome, a peripheral demyelinating neuropathy. Mutations in myelin protein genes cause
peripheral neuropathies (eg, Charcot­Marie­Tooth disease).

Neurotrophins (eg, NGF) are carried by retrograde transport to the neuronal cell body where they produce proteins associated with neuronal
development, growth, and survival and suppress neuronal apoptosis.

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