Neuronal activity-dependent myelin repair after stroke. (11th June 2019)

• Record Type: Journal Article
• Authors: Jia, Wanyi; Kamen, Yasmine; Pivonkova, Helena; Káradóttir, Ragnhildur T.
• Is Part Of: Neuroscience letters. Volume 703(2019)
• Page Start: 139
• Page End: 144
• Publication Date: 2019-06-11
• Subjects: Stroke -- Myelin -- Oligodendrocyte precursor cell -- Neuronal activity -- Myelination -- Neurotransmitter -- Glia; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2019.03.005
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: Neuronal activity regulates both remyelination and myelin plasticity. Enhancing myelin plasticity and remyelination may promote recovery after stroke. Remyelination and myelin plasticity depend on oligodendrocyte precursor cell states. Oligodendrocyte precursor cells are therapeutic targets for recovery after stroke. Abstract: Brain tissue undergoes substantial activity-dependent reorganisation after stroke due to neuronal plasticity, leading to partial functional recovery in patients. Concurrent myelin repair is crucial for proper neuronal network function and reorganisation. Myelin repair after stroke might occur as myelin plasticity or as remyelination through the recruitment and differentiation of oligodendrocyte precursor cells (OPCs), which become myelin-forming oligodendrocytes (OLs). These two processes might share a similar guiding mechanism, which is postulated to depend on neuronal activity and glutamate signaling to OPCs. However, with ageing, the ability of OPCs to differentiate into myelinating OLs decreases due to changes in their ion channel and neurotransmitter receptor expression profile, rendering them less sensitive to neuronal activity. Because of their unique ability to replace damaged OLs, OPCs represent a potential therapeutic target for myelin repair in the context of stroke.