It has been suggested that EGFR polarization within the membrane leads to actin colocalization and polymerization, and these processes in turn trigger cathodal galvanotaxis. Indeed the activation and polarization of EGFR toward the cathode-facing side of NPCs was demonstrated in. EGF has been extensively used to study NPC proliferation both in vitro and in vivo. Phosphoinositide 3-OH kinase (PI3K) is a well-known downstream effector of the EGFR. Rho GTPases (Rac1, Cdc42) are downstream targets of PI3K products and play key roles in the cytoskeleton remodeling process that is required for cell migration. Meng et al. demonstrated that pharmacological and genetic inhibition of PI3K signaling significantly attenuated embryonic and hippocampal adult NPC migration. Here we demonstrate that EGF also plays a role in the galvanotaxis of SE-derived NPCs. In the presence of the EGFR inhibitor erlotinib, undifferentiated NPCs experience significantly reduced migratory behaviour in the presence of a dcEF. However, their galvanotactic response is not completely eradicated in the presence of erlotinib, suggesting EGF is not exclusively responsible for NPC galvanotaxis. This is in line with the finding of Meng et al. that FGF receptors are also involved in NPC galvanotaxis. In contrast to their findings, however, SE-derived NPCs in the presence of bFGF alone exhibited a significant decrease in the velocity and directedness of migration ABT-199 citations compared to NPCs in the presence of both EGF and bFGF. This suggests that the mechanisms by which growth factors SB431542 ALK inhibitor mediate galvanotaxis may vary between hippocampal and SE-derived NPCs. The identification of neural stem cells in the adult brain has led to the development of endogenous neural precursor activation paradigms to repair the injured CNS. Critical to the success of such self-repair paradigms is the effective expansion and recruitment of NPCs to sites of injury or disease.