Myelin Plasticity and Repair: Neuro-Glial Choir Sets the Tuning

Abstract

The plasticity of the central nervous system (CNS) in response to neuronal activity has been suggested as early as 1894 by Cajal (1894). CNS plasticity has first been studied with a focus on neuronal structures. However, in the last decade, myelin plasticity has been unraveled as an adaptive mechanism of importance, in addition to the previously described processes of myelin repair. Indeed, it is now clear that myelin remodeling occurs along with life and adapts to the activity of neuronal networks. Until now, it has been considered as a two-part dialog between the neuron and the oligodendroglial lineage. However, other glial cell types might be at play in myelin plasticity. In the present review, we first summarize the key structural parameters for myelination, we then describe how neuronal activity modulates myelination and finally discuss how other glial cells could participate in myelinic adaptivity.

Neuron–Oligodendrocyte Communication in Myelination of Cortical GABAergic Cells

“…Can the structure of axonal myelin be adjusted to optimize conduction velocity and synaptic transmission? Communication between excitatory neurons and oligodendrocytes is now known to shape myelination and circuit maturation during experience- or learning-induced tasks in adults [ 4 , 123 , 217 , 218 , 219 ]. New myelin is formed and existing internodes are also remodeled, as well as the width of periaxonal space and the length of node of Ranvier [ 197 , 220 , 221 ].…”

Bexarotene normalizes chemotherapy-induced myelin decompaction and reverses cognitive and sensorimotor deficits in mice

“…Restoration of myelin damage as a result of cerebral insults or neurodegenerative processes is key to restoration of brain function. In the brain, myelin is produced by oligodendrocytes, while astrocytes, T cells and macrophages/microglia can all modulate myelin formation [15,29,45]. Retinoid X receptor (RXR) is a member of the NR2B nuclear receptor family.…”

Oligodendrocyte Dysfunction in Amyotrophic Lateral Sclerosis: Mechanisms and Therapeutic Perspectives

“…However, what governs OL decision to form initial sheaths and which axons to myelinate or remyelinate is not yet entirely clear. A lot of evidence supports the hypothesis that axonal parameters such as caliber, presence or absence of inhibitory signals, and activity-dependent secreted factors can regulate ensheathment fate [ 6 , 39 , 40 , 41 ], suggesting that myelination is the result of a highly orchestrated interaction between neurons and OLs. In this respect, Bechler and colleagues showed that myelinating cells of the CNS are able to sense axon diameter and in turn increase their sheath length on larger fibers.…”