Chronic Pain On/Off Switch Found

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Chronic Pain On/Off Switch Found

Discovery Raises Hope for Better Pain Treatments

By DeNoon

WebMD Medical News

Reviewed By Louise Chang, MD

on Thursday, July 27, 2006



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July 27, 2006 -- 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 Ambron,

PhD, said in a news release.

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.

SOURCES: Sung, Y.J. Neuroscience, August 2006; early online edition.

News release, Columbia University Medical Center.

http://www.webmd.com/content/article/125/116058