Commonly used antidepressants appear to target specific neurotransmitters in the brain that regulate chronic pain and depression-like symptoms, a newly understood mechanism that could shape future treatments for nerve pain and depression.
Published in the Proceedings of the National Academy of Sciences (PNAS), this study from researchers at the Icahn School of Medicine at Mount Sinai Medical Center used mice with chronic neuropathic pain to gain greater understanding of molecular pathways and antidepressant treatment for pain and depression. The molecular adaptations required for “recovery” from pain and depression are controlled by the gene RGS9 and RGS9-2, the protein it codes. Mice that lacked RGS9 responded significantly earlier to very low doses of antidepressants, had significant improvement of sensory deficits, and had no signs of depression-related behaviors. By inhibiting RGS9-2, the function of hundreds of other molecules vital for pain-relief and mood-elevation were also improved.
The results suggest that new therapeutic treatments targeting both the brain reward center as well as the previously identified pain-transmitting pathways in the spine could provide relief from chronic pain and depression, the authors concluded.
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This article originally appeared on MPR