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Chronic pain can continue long after an initial injury. When a nerve outside the brain and spinal cord (a peripheral nerve) is damaged and does not heal properly, it keeps sending constant pain signals. Over time, this nonstop bombardment of pain signals changes how your spinal cord and brain process information as sensory and emotion-associated circuits become hyperreactive, turning up the volume on pain.

Current pain treatments do not work well for everyone and can cause significant side effects. Painkillers like morphine just hide the pain, but researchers at Boston University Chobanian & Avedisian School of Medicine have identified the underlying problem.

They found that when they blocked a protein called RGS4 in the dorsal root ganglia innervating the lumbar spinal cord in an experimental model, the nervous system returned to a calm, normal state. The findings appear in the journal Science Signaling.

"Our findings suggest that one reason pain may become chronic is that sensory nerves themselves undergo molecular changes that keep them unusually sensitive," explains corresponding author Venetia Zachariou, Ph.D., Edward Avedisian Professor and chair of the department of pharmacology, physiology and biophysics at the school.

"By reducing RGS4 activity, our models were allowed to recover from abnormal pain sensitivity, while increasing RGS4 could make otherwise uninjured models more sensitive to pain.

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