Oligodendrocyte precursors (OPCs) originate at specific domains within the neural tube before migrating to colonize the entire CNS. Once in their target areas, these cells differentiate into oligodendrocytes, the myelin-forming cells in the CNS. Using the embryonic mouse optic nerve as an experimental model, we have analyzed the influence of FGF-2 on OPC development. FGF-2 exerts a dose-dependent motogenic effect on the migration of plp-dm20 + and it also acts as a chemoattractant on these cells. These effects produced by FGF-2 are principally mediated by the FGFR1 receptor, which is expressed by OPCs. Anosmin-1 is the protein that is defective in the X-linked form of human Kallmann syndrome. This protein is expressed by retinal axons and it also interacts with FGFR1, thereby impairing the migration of OPCs. Because both Anosmin-1 and FGF-2 are present in the optic nerve in vivo, we propose a model whereby the relative concentration of these two proteins modulates the migration of OPCs during development through their interaction with FGFR1. This FGF-2/FGFR1/Anosmin-1 system may be relevant in the context of demyelinating diseases.