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Toxin-Based Models to Investigate Demyelination and Remyelination

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Part of the book series: Methods in Molecular Biology ((MIMB,volume 1936))

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.

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Acknowledgments

Thanks to Natalia Murphy for consultation regarding the ethidium bromide protocol, and to Joseph Guy for performing the cuprizone brain MRI.

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Correspondence to Robin J. M. Franklin .

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McMurran, C.E., Zhao, C., Franklin, R.J.M. (2019). Toxin-Based Models to Investigate Demyelination and Remyelination. In: Lyons, D., Kegel, L. (eds) Oligodendrocytes. Methods in Molecular Biology, vol 1936. Humana Press, New York, NY. https://doi.org/10.1007/978-1-4939-9072-6_21

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