to astrocytes indicated that astrocytes significantly amplified the production of neurotoxic factors when exposed to microglia-conditioned media (Fig. 2J lane 2 to lane 6 and 7). This effect was further increased when expression of Nurr1 was reduced in astrocytes (Fig. 2J lane 3 to lane 8 and 9). We conclude that microglia are the initial responders to LPS-mediated inflammation and that astrocytes amplify the production of neurotoxic factors after the microglial activation. The knockdown of Nurr1 in either microglia or astrocytes increases the toxicity of CM, suggesting that Nurr1 inhibits the production of neurotoxic factors in both cell types.
