"stem cell niche" that retains the NSC's capacity of self-renewing and multipotency. Basic fibroblast growth factor (FGF2), hepatocyte growth factor (HGF), Notch-1, sonic hedgehog (SHH), noggin, ciliary neurotrophic factor (CNTF), and a soluble carbohydrate-binding protein, Galectin-1, are reported as factors that maintain such properties of NSC in stem cell niche. Like stem cells in SGZ, progenitor cells in SVZ also differentiate into neurons and form an intermediate cell called a transiently amplifying cell (TAC). A recent study revealed that beta-catenin signaling, Wnt β-catenin, regulates the differentiation of TAC. NSCs in the SVZ have a distinct capacity to migrate into the olfactory bulb in the anterior tip of the telencephalon by a pathway called the rostral migratory stream (RMS). This migration is unique to new neurons in the SVZ that embryonic neurogenesis and neurogenesis at other region of the brain are not able to perform. Another unique neurogenesis in the SVZ is neurogenesis by astrocytes. A study done by Doetsch (1999) showed that astrocytes in the SVZ can be dedifferentiate and differentiate into neurons in the olfactory bulb. Among four types of cells in the SVZ (migrating neuroblasts, immature precursors, astrocytes, and ependymal cells), migrating neuroblasts and immature precursors are silenced with the anti-mitotic agent and astrocytes are infected with a retrovirus. In the result, neurons that have the retrovirus are found in the olfactory bulb. Factors affecting neurogenesis Neurogenesis in the adult mammalian brain is affected by various factors, including exercise, stroke, brain insult and pharmacological treatments. For example, kainic acid-induced seizures, antidepressant (fluoxetine), neurotransmitters such as GABA and growth factors (fibroblast growth factors (FGFs), epidermal growth factor (EGF), neuregulins (NRGs), vascular endothelial growth factor (VEGF), and pigment epithelium-derived factor (PEDF) induce formation of neuroblasts. The final destination of NSCs is determined by "niche" signals. Wnt signaling drives NSCs to the formation of new neurons in the SGZ, whereas bone morphogenic proteins (BMPs) promote NSC differentiation into glia cells in the SVZ. However, in the case of brain injury, neurogenesis seems insufficient to repair damaged neurons. Thus, Cajal's theory was accepted for a long time. In actuality, in the intercranial physiological condition, many neurogenesis inhibitors are present (for example, axon growth-inhibitory ligands expressed in oligodendrocytes, myelin, NG2-glia, and reactive astrocytes in the lesion and degenerating tracts, and fibroblasts in scar tissue). The inhibitory ligands bind to growth cone receptors on a damaged neuron, which causes repulsion and collapse of the