The myelination of axons in the vertebrate nervous system through oligodendrocytes promotes efficient axonal conduction, which is required for the normal function of neurons. The central nervous system (CNS) can regenerate damaged myelin sheaths through the process of remyelination, but the failure of remyelination causes neurological disorders such as multiple sclerosis. In mammals, parenchymal oligodendrocyte progenitor cells (OPCs) are known to be the principal cell type responsible for remyelination in demyelinating diseases and traumatic injuries to the adult CNS. However, growing evidence suggests that neural stem cells (NSCs) are implicated in remyelination in animal models of demyelination. We have previously shown that olig2⁺ radial glia (RG) have the potential to function as NSCs to produce oligodendrocytes in adult zebrafish. In this study, we developed a zebrafish model of adult telencephalic injury to investigate cellular and molecular mechanisms underlying the regeneration of oligodendrocytes. Using this model, we showed that telencephalic injury induced the proliferation of olig2⁺ RG and parenchymal OPCs shortly after injury, which was followed by the regeneration of new oligodendrocytes in the adult zebrafish. We also showed that blocking Notch signaling promoted the proliferation of olig2⁺ RG and OPCs in the normal and injured telencephalon of adult zebrafish. Taken together, our data suggest that Notch-regulated proliferation of olig2⁺ RG and parenchymal OPCs is responsible for the regeneration of oligodendrocytes in the injured telencephalon of adult zebrafish.