Effects of IL-1β or arachidonic acid (AA) on neuronal survival in the presence of inflammation-activated glia in neuronal-glial cultures. Neuronal death was assessed by propidium iodide staining (PI; a) or chromatin condensation of neuronal nuclei (CC; b) after 6 days of treatment. Neuronal death was prevented by inhibitors of iNOS (25 μM 1400W), NADPH oxidase (1 mM apocynin), a blocker of the NMDA-receptor (10 μM MK-801) or a peroxynitrite scavenger (100 μM FeTPPS). Neuronal death was accompanied by proliferation of microglia (c). Microglial proliferation was inhibited by LPS/IFN-γ treatment alone but in the presence of IL-1β or AA it was stimulated and returned to basal levels. This stimulation of proliferation by IL-1β or AA (in the presence of LPS/IFN-γ) was completely prevented by apocynin. Additionally, nitrite/nitrate (NOX) levels correlated with the number of microglia present (d). Statistical differences were established using ANOVA at *p < 0.05, **p < 0.01 and ***p < 0.001, the symbol * is used when assessing prevention of neuronal death in comparison to LPS/IFN-γ with IL-1β or AA. The symbol ¶ is used when comparing neuronal death to that induced by LPS/IFN-γ alone and # when comparing neuronal death induced by IL-1β or AA treatment alone. In c & d, the differences are in comparison to IL-1β or AA alone (*), LPS/IFN-γ (¶) or LPS/IFN-γ plus IL-1β or AA (#). Data expressed is mean ± SEM, n = 3 or more.