Feb. 13, 2006 Researchers at the University of Illinois at Chicago have discovered that a long-approved oral antipsychotic drug can stop the addictive properties of opioid painkillers in mice.
The researchers injected a small dose (half a milligram) of trifluoperazine -- used in the treatment of mental diseases such as schizophrenia -- into laboratory mice hooked on morphine. After a few hours their addiction was gone, said Z. Jim Wang, assistant professor of pharmacology in the UIC College of Pharmacy.
This is the first time any study has shown the anti-addictive property of trifluoperazine, Wang said.
"From studies conducted in the 1970s and 1980s, we know that trifluoperazine inhibits calmodulin," Wang said, a molecule that is required for the activation of an enzyme called calcium/calmodulin-dependent protein kinase-2. "In previous studies we performed at UIC, we know that CaMK-2 plays an important role in the generation and maintenance of opioid tolerance," he said. Tolerance is a hallmark of drug dependence.
"Trifluoperazine targets this pathway, which then stops the addiction," Wang said. "When this occurs, you can still use a relatively low dose of the painkiller to achieve fairly good pain control and no drug dependence."
Opioids such as morphine are commonly used in pain management, but many patients are wary of taking them because of concerns over addiction or adverse side effects.
The study, which began early last year and was supported in part by grants from the National Institutes of Health and the American Foundation for Pharmaceutical Education, is published in the journal Neuroscience Letters. It is now available online and will be printed later this month.
Other researchers involved in the study were graduate student Lei Tang and post-doctoral researcher Pradeep Shukla, both of the UIC College of Pharmacy.
Other social bookmarking and sharing tools:
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Note: If no author is given, the source is cited instead.