Brain receptors may act as biological brakes on chronic pain after nerve injury
Deep at the base of the brain, a tiny cluster of nerve cells serves as the body's natural pain reliever, dialing down pain signals traveling up the spinal cord. But nerve damage can flip this system into a hyperactive engine for chronic pain.
At the base of the brain, a small cluster of nerve cells plays a role in naturally reducing pain signals travelling up the spinal cord. However, nerve damage can activate this system, causing chronic pain. Researchers at Washington University School of Medicine have discovered that specific receptors on cells in the brain's central alert and stress center act as biological brakes on pain.
These receptors, previously known to influence stress in this region, can turn off the pain engine to alleviate chronic neuropathic pain following nerve injury. The study, published in Current Biology, could lead to the development of targeted therapies that reduce chronic pain with fewer risks compared to traditional opioid medications.
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