that a u03b2o activated microglia and caused indirect microglia mediated neurotoxicity in hippocampal slices the treatment consisted of 20 nm a u03b2o for 24 hrs no was found to be a major inflammatory mediator released by a u03b2o stimulated microglia applicants tested whether no mediates neurotoxicity applicants used two selective inhibitors of inos n iminoethyl llysine l nil 57 and n 3 aminomethyl benzyl acetamidine 1400 w and found that both compounds significantly blocked the increased no release induced by a u03b2o fig8 a when a u03b2o treated microglia were concurrently treated with inos inhibitors their cm were no longer neurotoxic fig8 b when applied to cultured hippocampal slices 1 hr prior to a u03b2o application both inos inhibitors reduced no release fig8 c and inhibited neuronal damage as indicated by reduced pi uptake fig8 d more specifically in fig8 a no production was quantified as described in fig2 e the a u03b2o induced increase was prevented by 5 u03bcm 1400 w and 100 u03bcm l nil n 3 p lt 0 01 compared with the u201c a u03b2o u201d group in fig8 b a u03b2o induced microglial neurotoxicity was evaluated as described above with respect to fig5 control or a u03b2o treated microglia cultures were at the same time treated with vehicle 1400 w or l nil for 24 hrs hippocampal neuron cultures were then treated with 25 cm from each microglial culture neuronal viability was determined after 24 hrs both 1400 w and l nil blocked the a u03b2o induced microglial neurotoxicity n 3 p lt 0 001 compared with the u201c a u03b2ocm vehicle u201d group in fig8 c no released by hippocampal slices was measured as described.