May 14, 2026 - 13:32

University of Colorado Boulder researcher Linda Watkins is advancing her investigation into a biological mechanism she calls the "pain switch," a discovery that could reshape how chronic pain is understood and treated. In a recent update published in Science Daily, Watkins details how the body's immune system can inadvertently keep pain signals active long after an injury has healed.
Her work focuses on a specific receptor in the brain and spinal cord that, when triggered by immune cells, flips a switch from acute to chronic pain. Watkins explains that this process involves glial cells, which normally support nerve function, but can become overactive and release inflammatory chemicals. This creates a feedback loop where pain persists even without tissue damage.
The implications are significant for millions suffering from conditions like fibromyalgia, arthritis, and back pain. Watkins and her team are testing compounds that could "turn off" this switch by blocking the receptor's activation. Early animal studies show promise, with some subjects experiencing lasting relief without the side effects of opioids. Human trials are still years away, but Watkins emphasizes that understanding the switch offers a new target for drug development. She cautions that chronic pain is complex, but targeting this specific pathway could provide a more precise treatment option. The research continues to explore how stress and infection might also flip the switch, potentially explaining why some patients develop chronic pain after a viral illness.
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