Figures & data
Figure 1. A diagram showing the experimental protocol. Chemical sympathectomy with 6-hydroxydopamine (6-OHDA) (A), local capsaicin (CAP) treatment on the sciatic nerve (B), or pretreatment with systemic naloxone (NAX) (C) was performed before restraint stress. The baseline of PWMT and PV of rats were measured (PWMT & PV, test 1) 2 h prior to BV. BV was injected subcutaneously and the effects of different treatments on BV-induced spontaneous foot lifting were assessed continuously for 1 h. The PWMT and PV were then measured 2, 4, 8 h after BV (PWMT & PV, test 2–4) to assess the effects on BV-induced mechanical hyperalgesia and edema. At 9 h after BV treatment, rats in panels A were euthanized and noradrenaline (NA) levels were measured.
Figure 2. Effect of acute stress on BV-induced nociception and inflammation. Panel A shows the effect on BV-induced persistent SPFR; Panel B shows the effect on BV-induced decrease in PWMT; Panel C shows the effect on BV-induced increase in PV. One way ANOVA analysis shows that acute restraint stress attenuated significantly BV-induced SPFR and enhanced significantly BV-induced increase in PV, but had no effect on BV-induced increase in PWMT. *p < 0.05, **p < 0.01, ***p < 0.001. Values are mean ± SEM. One-way ANOVA with Tukey’s post-hoc tests, n = 10 for BV group; n = 10 for BV + Stress group.
Figure 3. Effect of local treatment of the sciatic nerve with capsaicin (CAP) on BV-induced PSN and inflammation under acute restraint stress. Panel A shows the effect on the inhibition of BV-induced SPFR produced by acute stress; Panel B shows the effect on the enhancement of BV-induced increase in PV produced by acute stress. Rats in Control groups were those treated with BV + Vehicle. One way ANOVA analysis shows that local CAP had no effect on acute stress-induced anti-nociceptive and pro-inflammatory effects. *p < 0.05, **p < 0.01, ***p < 0.001, compared with Control group; &p < 0.05, &&&p < 0.001, compared with BV + CAP group. Values are mean ± SEM. One-way ANOVA with Tukey’s post-hoc tests, n = 10 for Control group; n = 8 for BV + CAP group; n = 10 for BV + Stress group; n = 8 for BV + Stress + CAP group.
Figure 4. Effect of systemic treatment of 6-OHDA on BV-induced PSN and inflammation under acute restraint stress. Panel A shows the effect on the inhibition of BV-induced SPFR produced by acute stress; Panel B shows the effect on the enhancement of BV-induced increase in PV produced by acute stress. Rats in Control groups were those treated with BV + Vehicle. One way ANOVA analysis shows that systemic 6-OHDA had no effect on acute stress-induced anti-nociceptive effect, but reversed partially pro-inflammatory effects. *p < 0.05, **p < 0.01, ***p < 0.001, compared with Control group. Values are mean ± SEM. One-way ANOVA with Tukey’s post-hoc tests, n = 10 for Control group; n = 8 for BV + 6-OHDA group; n = 10 for BV + Stress group; n = 9 for BV + Stress + 6-OHDA group.
Figure 5. Effect of systemic naloxone (NAX) on BV-induced PSN and inflammation under acute restraint stress. Panel A shows the effect on the inhibition of BV-induced SPFR produced by acute stress; Panel B shows the effect on the enhancement of BV-induced decrease in PV produced by acute stress. Rats in Control groups were those treated with BV + Vehicle. One way ANOVA analysis shows that systemic NAX completely reversed the acute stress-induced anti-nociceptive effect, but had no effect on pro-inflammatory effects. *p < 0.05, **p < 0.01, ***p < 0.001 compared with Control group; ###p < 0.001 compared with BV + Stress group; &p < 0.05 compared with BV + NAX group. Values are mean ± SEM. One-way ANOVA with Tukey’s post-hoc tests, n = 10 for Control group; n = 8 for BV + NAX group; n = 10 for BV + Stress group; n = 10 for BV + Stress + NAX group.
