stimulation attenuates microglial proinflammatory cytokine release. Mouse primary microglial cells were seeded in 24-well tissue-culture plates (1 × 105/well) and co-treated with either IFN-γ (100 U/mL)/CD40L protein (2 μg/mL) or Aβ1–42 (1 μM)/CD40L protein (2 μg/mL) in the presence or absence of cannabinoid receptor CB2 agonist (JWH015, 5 μM) for 24 hr. Cell cultured supernatants were collected and subjected to TNF-α cytokine ELISA (A) and NO release assay (B) as indicated. TNF-α production was represented as mean pg of TNF-α per mg of total cellular protein (+/- SD). Similar results were obtained in three independent experiments. ANOVA and post hoc testing revealed significant differences between IFN-γ/CD40L and IFN-γ/CD40L and JWH-015 (** p < 0.005); Aβ1–42/CD40L and Aβ1–42/CD40L plus JWH-015 treatment (** p < 0.001).