TLR4 and ischemic stroke: TLR4 activation following exposure to LPS, an inflammatory mediator, negatively impacts hippocampal NPC proliferation, suggesting a detrimental effect of TLR4 on neurogenesis [7]; however, TLR4 activation in a model of ischemic stroke-induced NPC proliferation and survival within the subventricular zone promoted neural differentiation of migrating neuroblasts, suggesting a role in endogenous brain repair [19].