Resumo

Objectives: In the present study we monitored the plasma corticosterone level in two mouse strains submitted to acute and chronic pain models. In addition, a battery of behavioral tests and procedures commonly used in animal pain research was performed in other to evaluate the stress response under those conditions. Material and Methods: Experiments were performed using inbred male BALB/c/JUnib and C57BL/6/JUnib mice (20-25g). Acute pain was induced by unilateral capsaicin injection (10 µg/20µL, s.c.) in the dorsal aspect of the hindpaw. Sub-chronic inflammatory pain was developed by subcutaneous injection of λ-carrageenan (400µg/20µL) in the dorsal aspect of the left hind paw. Chronic inflammatory pain was induced by Complete Freund’s Adjuvant (CFA) injection (20 µl) in the dorsal aspect of hindpaw. Neuropathic pain was produced by a unilateral partial nerve injury of the sciatic nerve. At different time points, animals were euthanized and plasma corticosterone level measured by radioimmunoassay. The intra-assay error was 5% and the minimum detectable dose was 0.8 pg/ml. Behavioral tests were analysed by Mann-Whitney Test, whereas corticosterone assays were compared by Student t-test. Results: Thirty minutes after subcutaneous injection of either capsaicin and vehicle marked increased plasma corticosterone level in C57BL/6 and BALB/C strains compared to naïve animals (p<0.001), and vehicle-treated mice in both strains (p< 0.05). In C57Black/6 mice, plasma corticosterone level was increased only after 3 hours post-injection (p< 0.01), however, Balb/C animals showed increased corticosterone plasma level not only in the initial period of the inflammatory process but also 24 hours after carrageenan administration (p< 0.01). Corticosterone measurements revealed an increased plasma level for CFA-treated mice but not to vehicle-treated animals 3 h after injection (p< 0.01 compared to naïve animals). C57Black/6 mice showed a significant increase on plasma corticosterone levels 24h (p< 0.05) and 3 days post-injury (p< 0.01) whereas in Balb/C animals this increase occurred only 24 hours after injury (p< 0.01) compared to naïve mice. Intrathecal injection induced a significant increase on corticosterone level in both strains (p < 0.01). In addition, acute contact with the test apparatus for 30 minutes significantly increased the corticosterone level in both strains (p < 0.01). Unexpectedly, after 3 days of contact with the test apparatus the animals still respond with high plasma corticosterone levels after 30 minutes within the chamber (p < 0.01). Conclusion: In the present study indicate that different pain tests and the animal manipulation associated to them radically affect plasma corticosterone level in mice. In addition, the data strongly evidenced differences on stress response between two different mouse strains commonly used in experimental pain assays. In addition, our results suggest that the stress response under different pain conditions and environmental-related factors may strongly interfere with the outcome of any behavioral model of nociception leading to lack of across-laboratory replicability.