Incomplete remyelination via endogenous or therapeutically enhanced oligodendrogenesis is sufficient to recover visual cortical function.

Myelin loss induces deficits in action potential propagation that result in neural dysfunction and contribute to the pathophysiology of neurodegenerative diseases, injury conditions, and aging. Because remyelination is often incomplete, better understanding endogenous remyelination and developing remyelination therapies that seek to restore neural function are clinical imperatives. Here, we used two-photon microscopy and electrophysiology to study the dynamics of endogenous and therapeutic-induced cortical remyelination and functional recovery after cuprizone-mediated demyelination in mice.

Motor learning drives dynamic patterns of intermittent myelination on learning-activated axons.

Myelin plasticity occurs when newly formed and pre-existing oligodendrocytes remodel existing patterns of myelination. Myelin remodeling occurs in response to changes in neuronal activity and is required for learning and memory. However, the link between behavior-induced neuronal activity and circuit-specific changes in myelination remains unclear.