According to a news release from the University of Texas at Dallas (UT Dallas), the brain chemical dopamine is typically associated with cognition, movement, and reward-motivation behavior, but research from the university suggests that it may also play a role in promoting chronic pain. The paper was recently published in The Journal of Neuroscience.

The release notes that the study was led by Ji-Young Kim, a recent PhD graduate of the laboratory of Theodore Price, PhD, associate professor in the School of Behavioral and Brain Sciences at UT Dallas. During the study, the researchers followed the sequence of pain impulses traveling from the brain to the spinal cord in mice, the release notes. By removing a collection of neurons called A11 that contain dopamine, the release continues, chronic pain was selectively diminished.

Pain signals travel from the injury site to the spinal cord, where they pass on electrical or chemical pain signals to other cells, the release explains. These signals then travel upward and relay their information to the brain. There is no single pain center in the brain, the release says, however evidence suggests that chronic pain changes how these pain centers are activated.

In patients with chronic pain, the release reports, the neurons continue to send pain signals to the brain, even when there is no injury. The causes are reportedly unknown, but a potential explanation could be from A11. These neurons did not affect acute pain the release adds, yet researchers found that they had an effect on chronic pain. In their study, the release explains, researchers permanently reversed a chronic pain state by targeting these neurons in mice with chronic pain.

“These findings demonstrate a novel role for how dopamine contributes to maintaining chronic pain states,” Price says in the release. “This may open up new opportunities to target medicines that could reverse chronic pain.”

Previous studies have examined the role of other neurotransmitters—such as norepinephrine and serotonin—in chronic pain, Price adds.

“By the 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 notes.

According to the release, in 2011 the Institute of Medicine estimated that more than 100 million Americans suffer from chronic pain, which, it states, costs more than $600 billion per year in medial care and lost productivity. Therefore, understanding chronic pain and its contributing factors could potentially help lead to more effective treatments.

Price emphasizes that, in future studies, he and his team would like to gain a better understanding of how stress interacts with A11. He would also like to know more about the interaction between molecular mechanisms that promote chronic pain and dopamine.

[Source: University of Texas at Dallas]