A brain mechanism that could be a drug target to help prevent tolerance and addiction to opioid pain medication, such as morphine, has been identified according to a study by Georgia State University and Emory University.
The findings, published in the Nature journal Neuropsychopharmacology in August, show for the first time that morphine tolerance is due to an inflammatory response produced in the brain. This brain inflammation is caused by the release of cytokines, chemical messengers in the body that trigger an immune response, similar to a viral infection.
Researchers' results show blocking a particular cytokine eliminated morphine tolerance, and they were able to reduce the dose of morphine required to alleviate pain by half.
Over 67 percent of the United States population will experience chronic pain at some point in their lives. Morphine is the primary drug used to manage severe and chronic pain, with 3 to 4 percent of adults in the U.S. receiving long-term opioid therapy. However, tolerance to morphine, defined as a decrease in pain relief over time, significantly impedes treatment for about 60 percent of patients. Long-term treatment with opioids is associated with increased risk of abuse, dependence and fatal overdoses.
In the absence of pain, morphine interferes with the body's ability to maintain normal function, referred to as homeostasis. Anything that interferes with homeostasis is viewed by the body as a pathogen, resulting in an immune response to rid the body of the pathogen. When Eidson gave rats drugs that blocked the immune response, the rats no longer became tolerant to morphine.
The study also found that tolerance to morphine develops rapidly. Administering one dose of morphine to rats for three days was sufficient to induce tolerance.