A study conducted at the Icahn School of Medicine at Mount Sinai has advanced our understanding of the mechanisms underlying oxycodone action that may be of value in the effort to separate the analgesic effects of opioids from their addictive properties. The protein RGS9-2 is known to control the function of opioid receptors in the brain. Building on this knowledge, the research team employed mouse models of both acute and chronic pain to demonstrate that it promotes addiction to oxycodone in both pain states, as well as in pain-free conditions. However, mice that were genetically engineered to lack RGS9-2 encoding ability showed fewer addictive behaviors without affecting the analgesic properties of the oxycodone. The findings were published online earlier this week in the journal Neuropsychopharmacology.
An additional conclusion of the study was that the intracellular actions of oxycodone are distinct from those of morphine. Venetia Zachariou, PhD, Associate Professor at the Icahn School of Medicine at Mount Sinai, commented, “Our work reveals that intracellular factors that prevent the actions of morphine may actually promote the actions of oxycodone. This information is particularly important for pain management strategies, as a common course is to have patients oscillate between oxycodone and morphine to achieve pain relief.” The authors state that their work may assist clinicians in more accurately assessing the risks and benefits of oxycodone therapy for pain.
Read a news story about the discovery here.
The journal abstract may be read here.
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