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Molecules limit chronic nerve pain in rodents

Researchers from NIH, Saint Louis University School of Medicine, and other institutions have found that turning on a receptor in the brain and spinal cord counteracts chronic nerve pain in male and female rodents. Activating the A3 receptor—either by its native chemical stimulator, the small molecule adenosine, or by powerful synthetic drugs invented at the NIH—prevents or reverses pain that develops slowly from nerve damage. The A3 receptor limits chronic pain in mice and rats at multiple sites in their bodies in various ways, including boosting brain-to-spinal cord circuits that naturally decrease pain.

The findings may have implications for the treatment of diabetic neuropathy. Additionally, A3 receptor activators could be used with chemotherapy to avert or relieve chronic nerve pain, which is often a side effect of chemotherapy drugs and a reason life-saving chemotherapy is discontinued. Also, A3 receptor activators do not produce the tolerance seen with morphine, a drug commonly used for pain. More research is needed to determine effectiveness of this therapy in humans.

The studies published in Brain; Brain, Behavior, and Immunity; and Pain.

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