Fig. 2

Microglia proinflammatory activation participates in stress-related learning and memory dysfunction. (A) Representative images of microglia in the hippocampus. Scale bar, 5 μm (n = 3). (B) qRT-PCR assays monitoring expression of proinflammatory phenotype markers, CD86, IL-6, IL-1β, and TNF-α in hippocampal samples from CTRL and CUMS mice (n = 6, Student’s t-test). (C) qRT-PCR assays monitoring expression of anti-inflammatory phenotype markers, CD206, IL-10, Arg-1, and Ym1 in hippocampal samples from CTRL and CUMS mice (n = 6, Student’s t-test). (D) Representative images of IF staining of hippocampal sections from CTRL and CUMS mice. Iba-1, green; CD68, red; DAPI, blue. Scale bar, 50 μm (n = 3). (E) Levels of IL-6, IL-1β, and TNF-α in hippocampus lysates from CTRL and CUMS mice as determined by ELISA (n = 6, Student’s t-test). (F) Schematic timeline of CUMS, Minocycline treatment, and MWM test. (G) Escape latency to the platform during the training trials in MWM of CTRL, CUMS, and CUMS + Minocyciline (Mino) mice (n = 4, Two-way ANOVA with Tukey’s post hoc test). (H) Representative track images of mice in the probe trial of MWM. (I-K) Latency to enter the platform (I), swimming distance of first time to enter the platform (J), and platform crossings (K) in the probe trial of MWM of CTRL, CUMS, and CUMS + Mino mice (n = 4, One-way ANOVA with Tukey’s post hoc test). *p < 0.05, **p < 0.01