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Through glucorticoid signaling, the protein FKBP51 can regulate the perception of chronic but not acute pain in mice, scientists from University College London (UCL) and their colleagues have found. Stress and chronic pain can go hand in hand, yet much of how stress and chronic pain–related signaling are connected remains a mystery. Previously shown to be involved in responses to stress in humans and rodents, FKBP51 now appears to be a factor common to both processes. The results, published in Science Translational Medicine, point to FKBP51 as a potential therapeutic target to alleviate long-term, persistent pain.
“[The work] suggests that stress signaling, through the secretion of glucocorticoids, is an important regulator of chronic pain,” wrote Jaclyn Schwarz, a neuroimmunologist at the University of Delaware who was not involved in the study, in an email toThe Scientist. “The authors also confirm quite well . . . what has long been suspected: that the mechanisms underlying acute pain versus chronic pain are distinct.”
“This study suggests that changes in the glucocorticoid system and FKBP51 in the neurons of the spinal cord contribute to the switch from analgesia to hyperalgesia—or hypersensitivity to pain—and to the development of chronic pain,” said Samuel McLean, an associate professor of emergency medicine and anesthesia at the University of North Carolina School of Medicine who was not involved in the work.
Read full, original post: Blocking a Stress-Related Gene Relieves Chronic Pain
