Neuronal activity-dependent myelin repair after stroke.
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.
['Jia|Wanyi|W|', 'Kamen|Yasmine|Y|', 'Pivonkova|Helena|H|', 'Káradóttir|Ragnhildur T|RT|']
D000818:Animals D002454:Cell Differentiation D049109:Cell Proliferation D006801:Humans D009186:Myelin Sheath D058953:Neural Stem Cells D009473:Neuronal Plasticity D009474:Neurons D009836:Oligodendroglia D020521:Stroke
Myelin Myelin Stroke Oligodendrocyte precursor cell Neuronal activity Neurotransmitter Glia Myelination