In people with chronic pain, their nerve cells continue to send pain signals to the brain - even in the absence of injury.
Researchers from the University of Texas (UT) at Dallas and others traced the path of pain signals between the brain and spinal cord in mice and found removing a group of dopamine-containing cells selectively reduced chronic pain.
Senior author Ted Price, associate professor in behavioral and brain sciences at UT Dallas, says the study reveals a new role for dopamine in helping maintain chronic pain states, and suggests:
"This may open up new opportunities to target medicines that could reverse chronic pain."
In acute pain, when we suffer an injury, pain signals travel like electricity from the site of the injury to the spinal cord, which passes them on in the form of other chemical or electrical pulses that in turn are relayed to brain cells that distribute them throughout the brain.
In people with chronic pain, their nerve cells continue to send pain signals to the brain - even in the absence of injury - but the causes of this are not known.
The brain has several pain centers, and evidence suggests chronic pain alters how they are activated.
Targeting A11 dopamine-containing cells permanently reversed chronic pain in mice
The new study shows that a group of dopamine-containing cells called A11 do not affect acute pain, but they appear to have a profound effect on chronic pain.
In their paper, Prof. Price and colleagues describe how they permanently reversed a chronic pain state in mice by targeting A11 cells.
They got the idea for the study because they noticed other studies on chronic pain had looked at the role of other brain chemicals like norepinephrine and serotonin. So they decided to take a look at dopamine. Prof. Price explains what they did:
"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."
The researchers conclude their study increases our understanding of the causes of chronic pain and the factors that contribute to it, which should eventually lead to more effective treatments. Prof. Price adds:
"In future studies, we would like to gain a better understanding of how stress interacts with A11. And we'd like to know more about the interaction between molecular mechanisms that promote chronic pain and dopamine."
In 2011, the Institute of Medicine estimated that more than 100 million Americans suffer from chronic pain, amounting to a national burden of around $600 billion each year in medical care and lost productivity.
The University of Texas at Dallas, the National Institutes of Health and the Rita Allen Foundation helped fund the study.
Earlier this year, Medical News Today learned how another team at the University of Berne in Switzerland identified a brain mechanism that may be responsible for chronic pain. Writing in the journal Neuron, they explain how using mice they discovered that cells in the brain's gyrus cinguli appear to create a "pain memory."