Researchers from the University of North Carolina at Chapel Hill School of Medicine and the University of Helsinki found that Prostatic Acid Phosphatase, or PAP, was identical to another protein found on pain-sensing neurons that converts the chemical messengers that cause pain into ones that suppress it.

"This protein has the potential to be a groundbreaking treatment for pain and has previously not been studied in pain-sensing neurons," lead study author Mark J. Zylka, an assistant professor of cell and molecular physiology at UNC, said in a university news release.

The findings are to be published online this month in the journal Neuron.

When tested as a painkiller on mice, a single dose of the protein suppressed pain as effectively as morphine but lasted substantially longer. One dose of PAP lasted up to three days, much longer than the five hours gained with a single dose of morphine.

"We were really blown away that a simple injection could have such a potent effect on pain," Zylka said. "Not only that, but it appeared to work much better than the commonly used drug morphine."

The researchers found that PAP works by stripping away phosphate groups, the chemical tags that serve to activate or inactivate chemical messengers. In particular, it removes adenosine triphosphate, or ATP, which normally initiates the activities that invoke a painful sensation from adenosine monophosphate (AMP) in a neuron.

The researchers are checking to see if other proteins work similarly in these neurons. They are also trying to create molecules that interact with PAP to enhance or mimic its activity.