None of us is a stranger to pain. And though we all suffer from life’s occasional aches and pains, these are usually temporary and go away in a matter of hours or days.
Others are not so lucky. They experience chronic pain, a debilitating condition with no cure in which pain is a constant companion.
It is believed that in people with chronic pain signals from the brain, affecting how the body perceives pain, have somehow gone awry. Once turned on, they don’t turn off.
The discoveries of two different groups of researchers provide new details on the ways the brain handles chronic pain. This research not only sheds light on how people can best manage chronic pain, it will potentially lead to new pain relief treatments.
New details on the ways the brain handles chronic pain
In one study, published in the Journal of Neuroscience, researchers at the University of Bristol identified a biological basis for chronic spontaneous pain, which normally feels like a slow, burning sensation. The scientists discovered a particular protein channel, called TREK2, present in the sensory nerve fibers that detect spontaneous pain.
TREK2 typically acts as a “brake” in these nerve cells, limiting their activity and therefore limiting spontaneous pain. In people with chronic pain, the TREK2 channel isn’t synthesized as much, causing the nerve cells to fire all the time and contribute to the spontaneous burning pain.
The scientists also discovered that TREK2 synthesis is decreased after skin inflammation, a condition associated with nerve and organ damage that results in a specific type of chronic pain called neuropathic pain.
In another study, researchers at the Johns Hopkins University School of Medicine and the University of Maryland identified two molecules that appear to perpetuate chronic pain. These molecules also cause uninjured areas of the body to be more sensitive to pain when a nearby area has been hurt.
Using genetically engineered mice, the scientists induced pain on a system of pain-sensing nerves in the face called the trigeminal nerve. When one branch of the nerve was pinched for a long amount of time, the other branches were extra sensitive to additional pain.
In another part of the study, researchers bathed skin patches in the ear of mice with capsaicin, the active ingredient in hot peppers. Capsaicin usually activates a protein channel known as TRPV1, which is responsible for the sensation of pain in many nerve endings.
Not only were levels of TRPV1 elevated on branches of the nerve that were pinched, but also on uninjured branches that extended well beyond the pain site.
Next, the researchers performed a rescue experiment where they blocked production of serotonin, a neurochemical released by the brain during chronic pain. They discovered that blocking serotonin production reduced the elevation of TRPV1 channels on nerve endings.
This finding, published in Neuron, is promising for the future of pain therapeutics, since certain drugs that impact serotonin and TRPV1 have already been shown to be safe and effective in humans. Now they can be used to target chronic pain.
“With the identification of these molecules, we have some additional targets that we can try to block to decrease chronic pain,” an author of the study, Xinzhong Dong of Johns Hopkins, said in a statement.
February 7, 2014
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