Researchers at Columbia University in New York have identified a protein in nerve calls that acts as an “on/off switch for chronic pain.” They’ve applied for patents to develop a new class of drugs that they predict will block chronic pain by turning this switch off.
The “switch” is the enzyme protein kinase G (PKG), which is activated upon injury or inflammation. And, the researchers state, “we are 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.”
Scientists have known for years that for chronic pain to persist, “a master switch must be turned on” inside the first order
or peripheral nerve cells. These are the neurons that feed from the body to the second order
nerve cells in the spinal cord, responsible in turn for relaying pain messages to the brain.
Pain becomes chronic when the peripheral neurons continue to send pain messages even after damaged cells heal or inflammation in the tissue subsides. The pain switch does not turn off. But until now the identity of that switch in the peripheral neurons remained a mystery.
The discovery is important because previous approaches to alleviating chronic pain have focused on using drugs to damp the activity of the spinal cord neurons. That has proved hard to accomplish, because the drugs need to overcome the blood-brain barrier, which is a physical membrane that selectively controls passage of substances from the blood into the brain to protect and maintain a “stable brain environment.”
Further, the Columbia researchers note, none of the existing pharmaceutical drugs on the market are adequate to deal with chronic pain. “Cox-2 inhibitors carry severe risk of side effects, opioids are highly addictive, Tylenol is ineffective for chronic pain, and other pain drugs cause significant drowsiness,” they stated.
The article explaining this discovery, “Activation and retrograde transport of protein kinase G in rat nociceptive neurons after nerve injury and inflammation,”
by Y.J. Sung, et al., was published in the August 2006 issue of the journal Neuroscience