Abstract
Pain can be considered a specific stressor activating the same brain structures as other non-nociceptive stressors. On the other hand, stress has been found to be a powerful activator of descending antinociceptive system, which is mediated by opioid or non-opioid mechanisms in dependency on the stressor intensity.
These pain-modulating networks can cooperate synergically or potentiate themselves. Nevertheless, endogenous pain-modulating circuitry is not fixed; besides an inhibitory control there exists a descending facilitatory system.
The final effect of pain modulation depends on a balance between inhibitory and facilitatory inputs. We performed a pilot study testing the modulation of stress and pain by new substance TH-1212.