Skip to main content
. Author manuscript; available in PMC: 2016 Mar 1.
Published in final edited form as: Nat Neurosci. 2015 Jun 29;18(8):1081–1083. doi: 10.1038/nn.4053

Fig. 2. Mechanical allodynia after nerve injury is mediated by adaptive immune cells in female but not male mice.

Fig. 2

a) Reversal of mechanical allodynia after SNI by intrathecally administered glial inhibitors minocycline (MCL), fluorocitrate (FC) and propentofylline (PPF) in male but not female CD-1 mice, but in immunocompromised nude mice of both sexes. Bars represent mean ± SEM percentage of maximal anti-allodynia (n=4–7 mice/sex/drug/genotype). b) Male-specific reversal of allodynia from the PPARα ligand, fenofibrate (FFB) is blocked by the PPARα antagonist, GW6471, and by castration (TX). Bars as in graph a (n=4–6 mice/sex/condition). c) Female-specific reversal of allodynia from the PPARγ ligand, pioglitazone (PIO) is reversed by the PPARγ antagonist, GW9662, and by testosterone proprionate (TP). Bars as in graph a (n=7–10 mice/sex/condition). *p<0.05, **p<0.01 compared to corresponding female mice by t-test. •p<0.05, ••p<0.01, •••p<0.001 compared to same-sex wildtype (CD-1) or vehicle group by t-test. n.t. = not tested.