Fig. 5.
Stimulation of CD45-deficient microglia with Aβ peptides results in microglial activation. Primary cultured wild-type or CD45-deficient microglial cells were treated as indicated for 12 hr or co-cultured with primary cultured neuronal cells under the same treatment conditions for 36 hr. Control peptide is Aβ40-1. Microglial activation is evidenced by TNF-α production (mean ± 1 SEM; n = 3 for each condition presented) (a), NO assay (mean ± 1 SEM; n = 3 for each treatment condition) (b), and neuronal cell injury in co-culture experiments [mean LDH (percent) release ± 1 SEM;n = 3 for each condition presented] (c). For CD45-deficient microglia ina and b, one-way ANOVA revealed significant between-group differences (p < 0.001), and post hoc testing showed significant differences between control peptide and either Aβ1-40(p < 0.001) or Aβ1-42(p ≤ 0.001). For neuronal–CD45−/− microglial co-culture experiments, one-way ANOVA revealed significant between-group differences (p < 0.001), andpost hoc testing showed significant differences between control peptide and either Aβ1-40(p < 0.001) or Aβ1-42(p < 0.001).