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Toxin-Based Models to Investigate Demyelination and Remyelination.

Accepted version
Peer-reviewed

Type

Article

Change log

Authors

McMurran, Christopher E 
Franklin, Robin JM 

Abstract

Clinical myelin diseases, and our best experimental approximations, are complex entities in which demyelination and remyelination proceed unpredictably and concurrently. These features can make it difficult to identify mechanistic details. Toxin-based models offer lesions with predictable spatiotemporal patterns and relatively discrete phases of damage and repair: a simpler system to study the relevant biology and how this can be manipulated. Here, we discuss the most widely used toxin-based models, with a focus on lysolecithin, ethidium bromide, and cuprizone. This includes an overview of their respective mechanisms, strengths, and limitations and step-by-step protocols for their use.

Description

Keywords

Animal models, Cuprizone, Demyelination, Ethidium bromide, Lysolecithin, Lysophosphatidylcholine, Remyelination, Toxin, Animals, Cuprizone, Demyelinating Diseases, Disease Models, Animal, Ethidium, Lysophosphatidylcholines, Mice, Mice, Inbred C57BL, Rats, Remyelination

Journal Title

Methods Mol Biol

Conference Name

Journal ISSN

1064-3745
1940-6029

Volume Title

1936

Publisher

Springer New York
Sponsorship
Medical Research Council (MC_PC_12009)