Houston: A chemical in the brain associated with cognition, movement and reward-motivation behaviour may also play a role in promoting chronic pain, according to a new research.
Researchers at The University of Texas at Dallas said the chemical, dopamine, sets the stage for many important brain functions, but the mechanisms that cause it to contribute to chronic pain are less well understood.
In a study published in The Journal of Neuroscience, the researchers followed the sequence of pain impulses travelling from the brain to the spinal cord in mice.
They found that by removing a collection of neurons called A11 that contain dopamine, chronic pain was selectively diminished.
“These findings demonstrate a novel role for how dopamine contributes to maintaining chronic pain states,” said Dr Ted Price, associate professor in the School of Behavioral and Brain Sciences at UT Dallas.
“This may open up new opportunities to target medicines that could reverse chronic pain,” he said.
Pain signals travel like electricity from an injury to the spinal cord where they pass on electrical or chemical pain signals to other cells. Those pain signals then travel upward and relay that information to neurons in the brain where they can be distributed throughout.
There is no single pain centre in the brain, but there is substantial evidence that chronic pain changes how these pain centres are activated.
In people with chronic pain, neurons continue to send pain signals to the brain, even in the absence of injury, but the causes of this are not known. A potential explanation comes from A11.
These neurons didn’t affect acute pain, but they did have a profound effect on chronic pain, researchers found. By targeting these neurons in mice with chronic pain, the researchers permanently reversed a chronic pain state.
Price said that previous studies have examined the role of other neurotransmitters in chronic pain including norepinephrine and serotonin.
“By process of elimination, we decided to look more closely at dopamine. We used a toxin that affected A11 neurons, and that’s when we found that acute pain signals were still normal, but chronic pain was absent,” he said.
PTI
