Beschreibung
Myelination in CNS is a dynamic process that includes birth of oligodendrocyte progenitor cells, their differentiation into oligodendrocytes, and ensheathment of axons. Regulation of myelination by neuronal activity has emerged as a new mechanism of CNS plasticity. In this work, we used a mild contusive spinal cord injury (SCI) at T10, which demyelinates surviving axons of the dorsal corticospinal tract (dCST), to investigate the effects of induced neuronal activity on oligodendrogenesis, remyelination, and motor function after SCI. Neuronal activity was induced over the primary motor (M1) cortex. The activity increased the number of proliferating OPCs. Additionally, induced neuronal activity in the subchronic stages of SCI increased the number of oligodendrocytes, and enhanced myelin basic protein (MBP) expression and myelin sheath formation in dCST. The oligodendroglia regenerative response could have been mediated by axon-OPC synapses, the number of which increased after induced neuronal activity. Further, M1-induced neuronal activation promoted recovery of hindlimb motor function after SCI.
Autorenporträt
Dr. Qun Li is a neuroscientist in Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University. He has worked in spinal cord injury research for more than 20 years.
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