The paper, titled Constitutive Mu-Opioid Receptor Activity Leads to Long-term Endogenous Analgesia and Dependence, was authored by a team including lead author Bradley Taylor of the University of Kentucky College of Medicine Department of Physiology. Other authors include: Gregory Corder, Suzanne Doolen and Renee Donahue of the UK Department of Physiology; Brandon Jutras of the UK College of Medicine Department of Microbiology, Immunology and Molecular Genetics; Michelle Winter and Kenneth McCarson of the University of Kansas; Ying He, Zaijie Wang and Xiaoyu Hu of the University of Illinois; Jeffrey Wieskopf and Jeffrey Mogil of McGill University; and Daniel Storm of the University of Washington.
The scientists examined opioid function at sites of pain modulation in the spinal cord. When the opioids act at opioid receptor proteins, they “put the brakes” on the transmission of pain signals to the brain. For example, opioids are released when a patient undergoes surgery, a soldier is wounded in battle, or an athlete runs a marathon. Researchers have known for a while that blocking opioid receptors can increase the intensity of acute pain—the pain occurring immediately after injury. But up to this point, scientists had been unsure whether blocking opioids could increase chronic, long-term pain. They began their work with the idea that the opioid system is much more important than previously recognized, with an ability to indefinitely oppose chronic pain. If true, they reasoned, then blocking opioids should increase chronic pain.
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