Axonal Regulation of Central Nervous System Myelination: Structure and Function

I have never been able to figure out if demyelination occurs during stroke. Ask your doctor and get the protocol to remyelinate if needed.
http://journals.sagepub.com/doi/abs/10.1177/1073858417703030

Anna Klingseisen, David A. Lyons

First Published April 11, 2017 Review Article

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Abstract

Approximately half of the human brain consists of myelinated axons. Central nervous system (CNS) myelin is made by oligodendrocytes and is essential for nervous system formation, health, and function. Once thought simply as a static insulator that facilitated rapid impulse conduction, myelin is now known to be made and remodeled in to adult life. Oligodendrocytes have a remarkable capacity to differentiate by default, but many aspects of their development can be influenced by axons. However, how axons and oligodendrocytes interact and cooperate to regulate myelination in the CNS remains unclear. Here, we review recent advances in our understanding of how such interactions generate the complexity of myelination known to exist in vivo. We highlight intriguing results that indicate that the cross-sectional size of an axon alone may regulate myelination to a surprising degree. We also review new studies, which have highlighted diversity in the myelination of axons of different neuronal subtypes and circuits, and structure-function relationships, which suggest that myelinated axons can be exquisitely fine-tuned to mediate precise conduction needs. We also discuss recent advances in our understanding of how neuronal activity regulates CNS myelination, and aim to provide an integrated overview of how axon-oligodendrocyte interactions sculpt neuronal circuit structure and function.

Effect of Rehabilitation on Oligodendrocyte Progenitor Cells in a Mouse Model of White Matter Stroke

Your doctor should be able to translate this into a stroke protocol. I don't give a shit that this was just done in mice, What is the downside?
http://www.neurology.org/content/86/16_Supplement/P5.224.short

1. Candace Borders₂,
2. Kwan Ng₃ and
3. S. Carmichael₁

+Show Affiliations

1. Published online before print April 8, 2015, Neurology April 5, 2016 vol. 86 no. 16 Supplement P5.224

• Abstract

Abstract

Objective: To determine the effect of rehabilitation on oligodendrocyte progenitor cell (OPC) activity and neural repair in a mouse model of white matter stroke (WMS). Background: Physical activity has profound effects on white matter function. In humans, exercise mitigates the effect of progressive WMS on gait. Moreover, constraint-induced repeated use of the affected arm in both stroke patients and animal models enhances recovery. OPCs, which can mature into myelinating oligodendrocytes, are potential mediators of white matter repair. OPC proliferation and myelination in rodent cortex are promoted by neuronal activity and environmental stimulation. However, the effects of a specific motor task (like those performed by post-stroke patients in rehabilitation) in WMS have not yet been studied. Here we evaluated the effect of a skilled reach task on OPC activity in WMS. Methods: Three- and 20-month-old mice were trained on a skilled reach task for three weeks. WMS was then induced in the subcortical white matter underlying the motor cortex contralateral to the trained limb via injection of a vasoconstrictor. Mice were then divided into two groups: three weeks of continued reach task (to model the skilled limb use employed in human neurorehabilitation), or no reach task. Functional recovery of the mice was quantified with a skilled forelimb eating task. Brain tissues were analyzed using immunohistochemistry. Results: Relative to mice receiving no post-stroke rehabilitation, the skilled reach mice show greater numbers of OPCs in subcortical white matter. The effect is more pronounced for 3-month-old mice compared to 20-month-old mice. Lineage tracing via immunohistochemistry suggests OPCs in the skilled reach group have increased potential to develop into mature oligodendrocytes. Conclusions: Rehabilitation with skilled reach after WMS in this mouse model potentiates two critical components of white matter repair: the number of OPCs, as well as their ability to mature.