- Posted by Austin Swim
- On October 1, 2015
- 0 Comments
A new study published in Biological Psychiatry demonstrates that a particular molecule in the body’s nervous system controls morphine receptor signaling in a small group of brain cells—a finding that could aid in the development of less addictive prescription pain medications.
The study was carried out by The Scripps Research Institute (TSRI) and lead researcher Kirill Martemyanov, an associate professor on the Florida campus of TSRI. Researchers were particularly interested in a molecule that is known for its central role in regulating G protein signaling (RGS) protein, which in turn controls the morphine receptor (mu opioid receptor). For the study, researchers used genetically modified animal models (mice) that lacked the RGS protein RGS7, an abundant protein in the brain, in order to observe what influence RGS7 has on the body, particularly when morphine is present. In the experiment, the mice could press a lever to receive an infusion of morphine. Researchers then looked at the number of lever presses to determine how much the mice liked the morphine. Based on observation, the mice that lacked RGS7 craved the drug much more than their control counterparts.
In fact, after a series of self-administered morphine doses, the mice lacking RGS7 saw increased pain relief, delayed tolerance, and heightened withdrawal. In other words, lacking the protein predisposed them to morphine addiction.
Lead researcher Kirill Martemyanov explained the role of the RGS7 protein this way: “The mu opioid receptor acts as a conductor of the drug’s effects, while RGS7 acts as a brake on the signal.” Martemyanov and his team observed that RGS7 seems to influence how morphine affects the body by regulating changes in excitability of neurons and plasticity of synapses (the ability of synapses to change their function).
Overall, the findings of this study make a promising push toward developing new pain medications that pose less risk for developing addiction. Research Associate Laurie P. Sutton, the first author of the study, stated, “This study reveals a unique modulatory role of RGS7 in a brain-region-specific action to morphine use and indicates RGS7 as a potential drug target. Pharmacological intervention at the level of RGS7 may reduce some of the detrimental side-effects associated with opiates.” Martemyanov added, “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.”