Toxin-Based Models to Investigate Demyelination and Remyelination

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.

Keywords: Animal models; Cuprizone; Demyelination; Ethidium bromide; Lysolecithin; Lysophosphatidylcholine; Remyelination; Toxin.