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Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: Neuronal aldosterone elicits a distinct genomic response in pain signaling molecules contributing to inflammatory pain

Fig. 7

Aldosterone synthase inhibitor FAD286 reversed the enhanced expression of pain signaling molecules TRPV1, CGRP, Nav1.8, and trkA immunoreactivity in nociceptive dorsal root ganglia (DRG) neurons as well as mechanical hyperalgesia during inflammatory pain. al Continuous i.t. aldosterone synthase inhibitor FAD286 infusion to rats with Freund’s complete adjuvant (FCA)-induced inflammation reversed the increased number of pain signaling molecules TRPV1- (ac), CGRP- (df), Nav1.8- (gi), or trkA- (jl) IR DRG neurons. (P < 0.05, two-tailed independent Student’s t test; n = 9–17) (Bar = 40 μm). Data are expressed as means ± SD. m Continuous i.t. aldosterone synthase inhibitor FAD286 infusion resulted in significant PPT elevations compared to baseline (0 min) indicating a reversal of FCA inflammation-induced mechanical hyperalgesia (P < 0.05, repeated measurement-ANOVA, followed by post-hoc Dunnett’s test; n = 6–10)

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