The functions of bFGF is achieved by binding to the fibroblast growth factor receptors (FGFRs), actived the MAPK, PI3K, PLCγpathways and immediate early genes or transcription.There are at least four structurally related high affinity FGFRs, and the downstream signaling pathways are also varied when bFGF binded with various FGFR.To investigate the mechanisms of bFGF-stimulation the DRG-NCSCs differentiated along schwann cells by studing the FGFR , the sign pathways and immediate early genes or transcription.RT-PCR and Western blot experiments showed that the level of receptor-lwas high and levels of receptor-2 and-3 were relatively weak.Results from the chemical cross-linking and immunoprecipitation experiments showed that bFGF mainly bound to the FGFR-1 under our experimental conditions.The results of westemblotting showed that the activity of ERK1/2 and PI3K were sustained during the bFGF-stimulated period in contrasted with the control.The results of mass-spectrum, western blot and transcription activation domain assay had proved that bFGF-stimulation caused DRG-NSCs differentiate along schwann cells through an ERK1/2-dependent pathway without influencing the proliferation and survival of differentiated cells within 24 hours.bFGF induced phosphorylation of ERK/2 or AKT, increase the transcription activator of c-Jun and decrease of the expression of Mash-1, a transcriptional factor known to participate never system development.Application of U0126, a specific inhibitor of MEK1/2 which are upstream to ERK1/2, suppressed the the transcription activator of c-Jun and prevented DRG-NSCs differentiation in response to bFGF.However, administration of LY294002, an inhibitor of PI3K, did not affect the effect of bFGF on the the transcription activator of c-Jun and DRG-NSCs differentiation.When bFGF acted on the DRG-NSCs differentiation surpass 24 hours, bFGF influence the proliferation and survival of differentiated cells through an ERK 1/2 and PI3K/AKT pathways.In a word, bFGF induced DRG-NSCs to differentiate along schwanns cell by binding FGFR1, leading to ERK1/2 phosphorylation, enhancing the transcription activator of c-Jun, and decreasing the expression of Mash-1.