In the brain of multiple sclerosis (MS) patients, the conduction block of axons due to demyelination and inflammation underlies early neurological symptoms, whereas axonal transection accounts for permanent deficits occurring during later disease stages. The beneficial function of myelin for the protection of the axonal compartment and network stability between neurons has been shown in numerous studies. Thus, rapid and adequate remyelination is an important factor for axonal patronage during neuroinflammatory conditions. In this review article, we discuss frequently used experimental in vivo and in vitro animal models to examine remyelination and repair in MS. The focus of the discussion is the relevance of the toxin model 'cuprizone' to study the pathology of demyelination and the physiology of remyelination. This also includes recent findings in this animal model which implicate that axonal damage is an ongoing process independent of the initiation of endogenous remyelination.