A molecular switch turns off chronic pain, Columbia University researchers report.

The switch is an enzyme called protein kinase G or PKG. When PKG gets stuck in the "on" position, nerve cells keep sending pain signals -- long after the injury that originally caused the pain has healed. Turning PKG off stops the pain, rats studies show.

"We're very optimistic that this discovery, and our continued research, will ultimately lead to a novel approach to pain relief for the millions suffering from chronic pain," researcher Richard Ambron, PhD, said in a news release.

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Ambron and colleague Ying-Ju Sung, PhD, have applied for patents on the pathway of chemical signals that turns PKG on. They've also applied for patents on several molecules that turn PKG off.

Some 48 million Americans suffer from long-lasting pain. Current pain drugs don't always work -- and when they do, they can have serious side effects such as drowsiness. It's hoped that the PKG discovery will lead to a new class of pain drugs that is more effective and has fewer side effects.

After injury, pain sensors in the body can lapse into a hyper-excited state. Long after the original injury is gone, these pain cells keep on sending intense pain signals. PKG, Ambron's team discovered, is responsible for this long-term hyper-excitability of pain sensors.

The finding is exciting, because current pain drugs affect the brain's ability to receive pain signals from the spinal cord. Drugs that affect PKG would work much farther down the pain-signal pathway -- in the periphery of the body and not in the brain.

The study appears in the August issue of the journal Neuroscience.

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By Daniel J. DeNoon, reviewed by Louise Chang, MD

SOURCES: Sung, Y.J. Neuroscience, August 2006; early online edition. News release, Columbia University Medical Center.