Results from a recently published study led by researchers from The University of Texas at Dallas (UT Dallas) may have a significant impact on the future directions of chronic pain research. The study entitled, “Spinal Dopaminergic Projections Control the Transition to Pathological Pain Plasticity via a D1/D5-Mediated Mechanism,” provides evidence that dopamine, an important brain chemical that is associated with cognition, movement, and reward centers, may also have a role in debilitating chronic pain. The research was published in the latest edition of The Journal of Neuroscience.
- Neuron: a specialized cell of the nervous system that transmits nerve impulses
- Neurotransmitters: are the brain chemicals that communicate information throughout our brain and body that relay signals between nerve cells (neurons)
According to the Institutes of Medicine, approximately 100 million Americans suffer with chronic pain annually. This condition is thought to be caused by neurons that continually send pain impulses to a patient’s brain even in the absence of injury or illness. Previous studies have shown that targeting these defective neurons is associated with lower pain stimulation.
About the Study:
In this study, the researchers targeted a group of neurons known as A11, that contain dopamine. In the experimental model, they removed A11 neurons in mice with induced chronic pain, alleviating the pain stimulation that these animals reacted to, thereby reversing the chronic pain state induced.
In a University press release, Dr. Ted Price, PhD., associate professor, School of Behavioral and Brain Sciences, UT Dallas and senior study author, explained, “These findings demonstrate a novel role for how dopamine contributes to maintaining chronic pain states. This may open up new opportunities to target medicines that could reverse chronic pain.”
When discussing the future direction the investigators plan to take, Dr. Price stated, “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 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.”
For patients and their healthcare providers the results from this study could help find future effective therapeutic options for this debilitating condition.