Background & Objective: It is reported that acute forced swimming stress induces analgesia immediately, and chronic stress induces hyperalgesia. Whereas in response to nociceptive stimulation, small-diameter C-fibers of the excitatory system in the dorsal horn of the spinal cord are activated, therefore, in the present study, the effects of C-fiber lesion in stress and dexamethasone-induced analgesia and hyperalgesia in acute and chronic forms were investigated using Tail-Flick test. Methods: Adults Wistar male rats (180-200 g) were assigned into three groups (n=7): C-normal (intact C-fibers), sham (received capsaicin vehicle at neonate stage) and C-lesion (received capsaicin at neonate stage). Forced swim stress (10 min/day) in water (18±1 ºC) was considered as acute stress and repeated daily forced swim stress as chronic stress, also single-dose of dexamethasone (2 mg/kg, i.p.) was considered as acute dexamethasone and repeated for three days as chronic dexamethasone. Neonatal capsaicin treatment was used for C-fibers depletion. The nociceptive thermal threshold was assessed using Tail-Flick test. Results: In C-lesion group, thermal pain sensitivity was reduced (P<0.001). Acute stress in C-normal group, reduced pain (P<0.001) and in C-lesion group, it caused deeper antinociception in Tail-Flick (P<0.001). Chronic stress and acute-chronic dexamethasone in C-normal group, created hyperalgesia (P<0.001) and induced analgesia in C-lesion groups (P<0.01). Conclusion: It seems that presence of C-fiber is so important in thermal pain transmission in Tail-Flick test; therefore, C-fiber lesion, reduces pain sensitivity (analgesia), increases antinociception effects of acute stress, decreases hyperalgesia of chronic-stress and acute-chronic dexamethasone.

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