Figure 3.

Corticosterone mimics the ability of stress to enhance epinephrine hyperalgesia. A, Dose–response relationships for hyperalgesia induced by intradermal injection of epinephrine show that pretreatment with intradermal corticosterone (1 μg/2.5 μl) enhanced responses to epinephrine, measured 24 h later. Corticosterone was injected in one paw (Cort), while vehicle was injected in the contralateral paw (vehicle). No effect was observed in untreated contralateral paws. There was a significant main effect of corticosterone-treatment on epinephrine hyperalgesia between the groups (F_(3,84) = 8.32; p < 0.001). Post hoc analysis showed significant enhancement of epinephrine hyperalgesia 24 h (n = 10) after corticosterone treatment compared with the vehicle-treated paws (n = 10) during the same time period (p = 0.004). Epinephrine hyperalgesia remained significantly enhanced in the corticosterone-treated paws 7 d after corticosterone injection (n = 6), whereas the vehicle-treated paws (n = 6) remained unaffected (p < 0.005). B, Intradermal corticosterone did not significantly increase sound stress enhancement of epinephrine hyperalgesia compatible with an occlusion of overlapping mechanisms. There was a significant main effect of corticosterone treatment on epinephrine hyperalgesia (F_(3,144) = 32.4; p < 0.001). Post hoc analysis showed that corticosterone treatment did not further enhance epinephrine hyperalgesia 14 d after sound stress (n = 10) compared with sound stress with (p > 0.05; n = 10) or without (p > 0.05; n = 20) corticosterone vehicle. Error bars indicate SEM.