Fig. 9

CXCL13 induces CXCR5/ERK-dependent release of pro-inflammatory cytokines in mouse hippocampus. WT or CXCR5^−/− mice received CXCL13 via intracerebroventricular injection. Seven days later, Barnes maze and fear conditioning tests were conducted. a Time to identify the target hole during training sessions and b latency time during memory phase were measured in the Barnes maze. Freezing times were quantified c in context and d in response to a cue. e Western blotting and densitometry of hippocampal p-ERK, total ERK, IL-1β, and TNF-α. Mice were injected with CXCL13 with or without PD98059 pretreatment, and behavioral tests were performed 7 days later. f Time to identify the target hole in training sessions and h latency time in memory phases of the Barnes maze. Freezing times were quantified i in context and j in response to a cue in fear conditioning tests. k Western blot and densitometry of IL-1β and TNF-α. All quantitative results (mean ± SD) shown were obtained with n = 8 animals per group. *P < 0.05 vs. vehicle + WT; ^#P < 0.05 vs. CXCL13 + WT; ^$P < 0.05 vs. vehicle; ^&P < 0.05 vs. CXCL13. CXCL13 C-X-C motif chemokine 13, CXCR5 C-X-C motif chemokine receptor 5, WT wild-type, TNF-α tumor necrosis factor alpha, IL-1β interleukin-1 beta