Fig. 7
New oligodendrocyte and Schwann cell myelination after SCI and its relationship to locomotor recovery. a Schematic of the uninjured and injured mouse spinal cord two and six WPI following moderate dorsal thoracic contusion. In the uninjured spinal cord, axons are myelinated solely by oligodendrocytes and peripheral nerves are myelinated by Schwann cells. By two WPI, the lesion epicenter is ringed by a glial scar and mostly devoid of axons. Demyelinated axons are seen in a gradient increasing outwards from the medial spinal cord. By six WPI, extensive oligodendrocyte remyelination is observed throughout the ventrolateral white matter in control mice with functional MYRF, but Myrf ICKO mice fail to produce new oligodendrocyte myelin. Schwann cell myelination is generally confined to the dorsal column. The degree of Schwann cell myelination does not differ in the injured spinal cord between Myrf ICKO and control mice. b Diagram illustrating the relative amount and rate of open field hindlimb motor performance compared to the extent of oligodendrocyte and Schwann cell myelin after injury in the spinal cord. After thoracic SCI, there is a decline in both hindlimb motor performance and number of myelinated axons in the CNS. The majority of recovery of hindlimb locomotor function on open field testing occurs within the first two weeks in both Myrf ICKO and controls. In contrast, the vast majority oligodendrocyte remyelination does not occur until after two weeks postinjury. Therefore, the relative time course of oligodendrocyte remyelination is not associated with hindlimb motor recovery after SCI. In contrast, Schwann cell myelination occurs within the first two weeks after SCI and occurs at a relatively steady rate. The height of the lines is approximately proportional to the extent of loss and subsequent recovery after SCI
