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. Author manuscript; available in PMC: 2010 Aug 1.
Published in final edited form as: Brain Behav Immun. 2009 Apr 8;23(6):851–860. doi: 10.1016/j.bbi.2009.04.001

Figure 1.

Figure 1

Stress and corticosterone exacerbate nerve-injury induced allodynia. A) Acute stress (60 min restraint) increases plasma CORT (vs. No Stress (NS)). By binding GR, RU486 treatment increases plasma CORT (vs. Vehicle (Veh)). CORT treatment also increases plasma CORT (vs. Veh). B) Acute stress prior to SNI decreases the pain threshold (von Frey hair measurements) in the ipsilateral hind paw on post-SNI days 1, 3, 5, & 7 compared to the NS group. Stress has no effect on sham-operated mice (vs. NS; black circle = Sham NS; white circle = Sham Stress). C) When RU486 (RU) was used to block GRs, stress-induced potentiation of mechanical allodynia is reduced on post-SNI days 1 & 3 compared to Veh, as indicated by “##.” Asterisks (*) indicate the difference between Veh + NS and Veh + Stress allodynia on post-SNI days 1, 3, 5, & 7. D) Treatment with CORT prior to SNI decreases the pain threshold in the ipsilateral hind paw on post-SNI days 1, 3, 5, & 7 compared to Veh. Compared to Baseline (BL), CORT reduces pre-SNI thresholds (#p<0.0001). Results are expressed as the mean ± SEM; B,C,D; n=5-6/group SNI, n=2/group Sham; y-axis values represent von Frey hair handle markings. *p<0.05; ** or ##p<0.01;***p<0.0001.