Erkl/2 but not PI3K Pathway Is Required for Neurotrophin 3-Induced Oligodendrocyte Differentiation of Postnatal Neural Stem Using cultured postnatal hippocampal stem cells (NSCs) as a model, we demonstrated that NT3-stimulation causes NSCs to differentiate into OLPs through an Erkl/2-dependent pathway without influencing the proliferation and survival of OLPs. NT3 induced phosphorylation of Erkl/2 or Akt and increase of expression of Olig-1, a transcriptional factor known to participate in oligodendrocyte development. Application of U0126, a specific inhibitor of MEK1/2 which are upstream to Erkl/2, suppressed the expression of Olig-1 and prevented NSC differentiation into OLPs in response to NT3 stimulation. However, administration of LY294002, an inhibitor of PI3K which are upstream to Akt, did not affect the effect of NT3 on the expression of Olig-1 and on NSC differentiation into OLPs. These results suggest that NT3 induce NSCs to differentiate into OLPs by enhancing the expression of Olig-1 through an Erkl/2-dependent pathway. Collaboration of NT3 and bFGF Increased Nuclear Translocation of TrkC whereas Enhanced Interaction between FGFR1 and TrkC during the Differentiation of Postnatal Neural Stem Cells Using cultured postnatal hippocampal NSCs as a model, we demonstrated that TrkC translocated into nucleus during the differentiation of neural stem cells. Immunocytochemical results showed that TrkC were located on the plasma membrane within 24 hours however, began to translocate into nucleus within 72 hours of the differentiation of NSCs. Using specific antibodies that recognize extracellular or intracellular domain of TrkC respectively, we found that TrkC translocated into nucleus in a short-length isoform which lose N-terminal structure. NT3 upregulated nuclear translocation of TrkC in the presence of bFGF. Co-immunoprecipitation result demonstrated that collaboration of bFGF and NT3 enhanced interaction between FGFR1 and TrkC, which might be involved in nuclear translocation of TrkC. In short, we reported nuclear translocation of TrkC for the first time, which might be dependent on the interaction between FGFR1 and TrkC during the differentiation of NSCs.