A new study appearing this month in the Proceedings of the National Academy of Sciences (PNAS) finds that commonly prescribed antidepressants alter a key signaling protein in the brain that processes both pain and mood. Conducted by researchers at the Icahn School of Medicine at Mount Sinai, the findings are termed significant for the insights offered into the brain’s reward system that may facilitate the development of better treatment options for both pain and depression. The study focused on mice suffering from chronic neuropathic pain, a condition often related to diabetes, infection, or trauma—and which persists even after the original source of the pain is gone. This pain often leads to depression, but brain mechanisms underlying this connection were previously unknown, as were the mechanisms by which common antidepressant drug classes—tricyclic (TCA) antidepressants or selective serotonin norepinephrine inhibitors (SNRIs)—counter both pain and depression related symptoms.
The study suggests that antidepressants that target monoamines, signaling chemicals in the brain that regulate chronic pain and depression, act in the nucleus accumbens, a part of the brain’s reward system, and likely through pathways that pass on messages to nerve cells through a controlling protein, RGS9-2. Antidepressant medications are increasingly prescribed for neuropathic pain, as they lack the addictive potential of opioids, and are more effective for these pain conditions.
Read more about the study findings here.
The journal abstract may be read here.