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Nervous Tissue: Myelin

Nervous Tissue: Myelin

The myelin sheath is a multilayered lipid and protein covering that insulates the axon of a neuron, enhancing the speed of nerve impulse conduction. Axons without this sheath are referred to as unmyelinated. Two types of neuroglia, Schwann cells in the peripheral nervous system (PNS) and oligodendrocytes in the central nervous system (CNS) are responsible for producing myelin sheaths.
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Neurons communicate by firing action potentials—the electrochemical signal that is propagated along the axon. The signal results in the release of neurotransmitters at axon terminals, thereby transmitting information to the nervous system. An action potential is a specific "all-or-none" change in membrane potential that results in a rapid spike in voltage.
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Related Experiment Video

Updated: Jul 5, 2026

Experimental Demyelination and Remyelination of Murine Spinal Cord by Focal Injection of Lysolecithin

Experimental Demyelination and Remyelination of Murine Spinal Cord by Focal Injection of Lysolecithin

Published on: March 26, 2015

Remyelination protects axons from demyelination-associated axon degeneration.

K A Irvine¹, W F Blakemore

¹Department of Veterinary Medicine, MS Society Cambridge Centre for Myelin Repair, Madingley Road, Cambridge, CB3 OES, UK. karen.irvine@ucsf.edu

Brain : a Journal of Neurology

|May 21, 2008

Summary

Prompt remyelination protects axons from damage in multiple sclerosis. Failure to remyelinate accelerates axonal degeneration, highlighting remyelination

Related Experiment Videos

Last Updated: Jul 5, 2026

Experimental Demyelination and Remyelination of Murine Spinal Cord by Focal Injection of Lysolecithin

Experimental Demyelination and Remyelination of Murine Spinal Cord by Focal Injection of Lysolecithin

Published on: March 26, 2015

Area of Science:

Neuroscience
Neuroimmunology
Cell Biology

Background:

Demyelination in multiple sclerosis (MS) leads to axonal injury and neurological disability.
Mechanisms of axonal degeneration in MS are not fully understood, with remyelination failure being a key hypothesis.
Axonal loss is the primary driver of irreversible disability in MS.

Purpose of the Study:

To test the hypothesis that failed remyelination contributes to axonal degeneration after demyelination.
To investigate the role of remyelination in protecting axons from demyelination-associated injury.

Main Methods:

Inhibiting remyelination using X-irradiation prior to cuprizone intoxication in a mouse model.
Assessing axonal degeneration and loss in irradiated versus non-irradiated mice.
Restoring remyelination capacity by transplanting neural progenitors into irradiated mice.

Main Results:

X-irradiation significantly increased axonal degeneration and loss in cuprizone-intoxicated mice.
Restoring remyelination capacity via neural progenitor transplantation significantly improved axon survival.
These findings demonstrate a direct link between remyelination failure and axonal loss.

Conclusions:

Prompt remyelination is crucial for protecting axons from demyelination-associated damage.
Failure of remyelination significantly contributes to axon loss observed in multiple sclerosis.
Enhancing remyelination holds therapeutic potential for mitigating MS-related neurological disability.