SDF-1α has been implicated in the post-traumatic neuroinflammatory cascade. We quantified the effect of SDF-1α on neural stem cell proliferation and differentiation. We found that the SDF-1α-CXCR4 axis can be manipulated so that the proliferative capacity of this chemokine can be separated and controlled. We have successfully modulated the proliferative activity of SDF-1α by preventing its binding to CXCR4. However this is an all-or-nothing approach. To achieve more precise modulation in future experiments, we will employ agonists and antagonists that modulate the downstream targets of this chemokine.