During development, NP cells in the hippocampus are exposed to a variety of cues with different effects, which are integrated by NP cells so that an appropriate number of cells are ultimately generated. It is therefore important to understand the antagonism and cooperation between cellular factors and the mechanism underlying. In this dissertation, using an FGF2-dependent rat neurosphere culture system, we found that NT3 inhibited both FGF2-induced neurosphere growth and bromodeoxyuridine (BrdU) incorporation in a dose-dependent manner. U0126, a MEK1/2 inhibitor, and LY294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor, both inhibited BrdU incorporation induced by FGF2, suggesting that the extracellular signal-regulated kinasel/2 (ERK1/2) and PI3K pathways are required for FGF2-induced neural progenitor cell proliferation. We found that NT3 significantly inhibited FGF2-induced phosphoryiation of Akt and glycogen synthase kinase3p (GSK3(3), a downstream kinase of Akt, whereas NT3 did not affect phosphoryiation of ERK1/2. The inhibitory effect of NT3 on FGF2-induced neural progenitor cell proliferation was abolished by LY294002 and treatment of SB216763, a specific glycogen synthase kinase 3 (GSK3) inhibitor, prevented the inhibitory effect of NT3 on FGF2-induced NP cell proliferation and rescued both neurosphere growth and BrdU incorporation. Moreover, experiments with Anti-NT3 antibody showed that endogenous NT3 also played a role in inhibiting FGF2-induced NP cell proliferation and that the Anti-NT3 antibody enhanced phospho-Akt and phospho-GSK3(3 levels in the presence of FGF2. These findings indicate that FGF2-induced NP cell proliferation is inhibited by NT3 via the PI3K /GSK3 pathway. The second set of experiment is to study the role of NT3 and FGF2 in the differentiation of neural stem cell. Under appripriate conditions, multipotential neural stem cell can differentiate to neuron, astrocyte, or oligodendrocyte. Experiment results show that the addition of NT3 or FGF2 alone induces neural stem cell to differentiate to oligodendrocyte. While the ratio of oligodendrocyte decreased to the base level when NT3 and FGF2 were added together. Thus an antagonism exits between the actions of NT3 and FGF2 on oligodendrocyte differentiation.