According to a new study in Biological Psychiatry, scientists have nowidentified a key morphine regulator in the brain and that finding could lead to the development of less-addictive painkillers.
Morphine achieves its euphoric effect by acting on a particular receptor protein, but previously the regulation of that protein had not been thoroughly understood. But new research by Kirill Martemyanov of The Scripps Research Institute has identified the specific molecule that controls the signaling to that morphine receptor protein.
The protein, RGS7, is abundant in the brain and it controls the mu opioid receptor, or morphine receptor. For this study, scientists looked at what would happen if that regulating protein were removed.
Using animals that were genetically modified to eliminate that particular protein, scientists found that a lack of RGS7 results in increased pain relief, delayed tolerance, and increased withdrawal. That means there’s more reward and increased dependence for animals lacking RGS7.
The net result is that animals without RGS7 are more likely to become morphine addicts.
“The mu opioid receptor acts as a conductor of the drug’s effects while RGS7 acts as a brake on the signal,” Martemyanov said. “The animals could press a lever to receive an infusion of morphine. We looked at the number of lever presses to determine how much they liked it and, judging from this test, mice lacking RGS7 craved the drug much more than their normal siblings.”
The study hasn’t been replicated in humans yet, but Martemyanov said, “If our findings hold true for human patients, you could look specifically for RGS7 levels for any disabling mutation with a simple blood test.”
“Mutations could indicate a strong reaction to a drug such as morphine—people carrying a deficient copy of the RGS7 gene might need much lower doses of opioids and could be cautioned to be extra careful with these substances.”
This could mean a genetic test for opioid addiction is in the not-too-distant future.
This story was originally published on The Fix.