Many modern opioid-based painkillers don't target the specific site of pain but instead interfere with the brain's sensation of that pain. It's not an especially efficient way to tackle pain and has resulted in widespread social problems stemming from the addictive quality of the drugs. A team of researchers has revealed a novel method for reducing our responsiveness to pain and it involves tricking our body's pain-signaling processes.

A great deal of research is currently underway to find effective and viable new techniques to control pain without resorting to addictive and psychoactive opioids. Some scientists are looking to nature, inspired by the venom of sea snails or the unusual anatomy of poisonous frogs. Other research is looking inward at human beings with unique genetic mutations that cause them to feel no pain. This new study looks at pain from a different perspective, focusing on how the body communicates the signals for pain on a molecular level.

"When you have an injury, certain molecules are made rapidly," says Zachary Campbell, from the The University of Texas at Dallas. "With this Achilles' heel in mind, we set out to sabotage the normal series of events that produce pain at the site of an injury. In essence, we eliminate the potential for a pathological pain state to emerge."

The pain we feel from inflammation or injury is communicated to the brain by a set of pain-signaling proteins. These proteins are produced as directed by messenger molecules called mRNA, provided by a cell's genome. The new research has identified a way to inject a compound at the site of an injury that effectively acts as an RNA mimic, disrupting the process that produces the pain-signaling proteins and communicating to the rest of the body that everything is essentially OK.

"We're manipulating one step of protein synthesis," says Campbell. "Our results indicate that local treatment with the decoy can prevent pain and inflammation brought about by a tissue injury."

Across several experiments on mice the RNA mimic molecule was successfully found to reduce the animal's behavioral response to pain. Campbell says this is the first time anyone has created a compound that can successfully disrupt RNA-protein interactions and the implications of the research could be much more broad than just a new pain-relieving drug.

"Our approach suggests that targeting those interactions may provide a new source of pharmacological agents," says Campbell. "This proof of concept allows us to open a whole new area of science by virtue of the route that we're attacking it."

The study was published in the journal Nature Communications.