Anti-depressants may be effective in treating pain because they decrease NF-kappaB activation in the brain
In the study summarized below, mirtazapine (an anti-depressant) is found to inhibit NF-kappaB activation in the brain, thereby reducing inflammation and the mediators of inflammation in the brain.
Repeated administration of mirtazapine inhibits development of hyperalgesia/allodynia and activation of NF-kappaB in a rat model of neuropathic pain
Summary of the abstract
Antidepressants have been widely used to treat neuropathic pain for many years. (Some benefit has also been reported in fibromyalgia patients.) However, the mechanisms of their analgesic actions are little known and remain controvertible.
Recent studies indicate that cytokines in central nervous system (CNS) play a critical role in the pathological states of pain. The present study was designed to explore the effects and most appropriate dosage of mirtazapine in treating neuropathic pain and its possible neuroimmune mechanisms.
The inflammatory cytokines production such as TNFalpha, IL-1beta, IL-10 and nuclear factor kappa B (NF-kappaB) activity in brain was determined. We found that mirtazapine can markedly attenuate mechanical and thermal hyperalgesia (excessive pain) produced by nerve transection (cutting the nerve), most significantly on the 14th day.
The elevated TNFalpha, IL-1beta and NF-kappaB in brain were accordingly reduced, while the expression of increased IL-10 were even stimulated after repeated mirtazapine administration.
Our data could conclude that mirtazapine suppressed neuropathic pain partially through inhibiting cerebral proinflammatory cytokines production and NF-kappaB activation in CNS.