Chronic pain affects millions of people, but many of the medications to treat it are either not very effective or have unpleasant side effects. Richard Ambron from Columbia University in New York City says pain is not necessary. "Means should be developed to minimize pain," he insists, "both to affect the quality of life for people who have chronic pain and also to alleviate pain for people who are dying."
So he and his fellow researchers looked at the mechanisms of pain at the molecular and the cellular levels. Ambron says these mechanisms control how nerves send pain signals to the brain. "What happens in a chronic pain state," Ambron explains, "is that the neurons become hyper-excitable. That is, rather than remaining rather dormant and unresponsive, they begin to fire in response to very, very mild stimuli. So we were interested in what is it that causes this hyper-excitability."
On the molecular level, they found what they think is the key enzyme that causes nerve cells to remain hyper-excited. The nerves then continue to communicate pain to the central nervous system, even when the cause of the pain has been removed. "Since we now know one of the key molecules that creates this hyper-excited state, if we can target that molecule with a drug to shut it off, then we will shut down the pain." Ambron says knowing about this 'master switch' for chronic pain will help researchers develop treatments to turn the switch 'off.'