ABSTRACT
Stimulation of peripheral nociceptors leads to releasing of some mediators such as substance P (SP) and Calcitonin gene-related peptide (CGRP) and contributes to the edema formation by vasodilatation induction. On the other hand glucocorticoids have anti-inflammatory action, and they are elevated in the plasma during stress. This communication reports C-fibers inflammatory role and the effects of chronic and acute stress and/or dexamethasone (as stress mimicry) on paw edema induced by formalin at presence/deficit C-fibers rats. Acute stress and dexamethasone and chronic dexamethasone have shown an anti-inflammatory effect in C-normal groups, but chronic stress had no effect on inflammation. C-fibers reduction (C-lesion) had anti-inflammatory effects. In deficit C-fibers rats, acute and chronic stress had not stronger anti-inflammatory effect, but acute dexamethasone reduced the anti-inflammatory effect of C-fibers reduction while in the same condition, chronic dexamethasone induced stronger anti-inflammatory effect. The results show C-fiber nerve produce and release the peripheral inflammatory mediators, "C-fibers reduction" decreased the paw inflammation. Counter adaptation in C-lesion animals may reduce the modulatory effects of dexamethasone on the remaining C-fibers. Acute dexamethasone diminished the "C-fibers reduction" anti-inflammatory effect, but at chronic treatment, the modulatory effects of dexamethasone aggregated and it augmented the C-fibers reduction anti-inflammatory effect.