Dopamine May Be Key To Unlocking Chronic Pain

DopamineMedical researchers at the University of Texas say dopamine – the mechanism in your brain responsible for movement, memory and reward – could provide the key to unlocking the problem of chronic pain.

Dopamine is vital for several different brain functions, but its contributions to the problem of chronic pain are not well known. To better understand dopamine’s role in chronic pain transmission, researchers began studying its effect in mice. Researchers noted that removing a specific collection of neurons -known as A11 – helped diminish the perception of chronic pain. The cluster of A11 neurons contained high levels of dopamine.

“These findings demonstrate a novel role for how dopamine contributes to maintaining chronic pain states,” said associate professor Dr. Ted Price.

How it Works

When a person gets injured, neurons inside the body send pain signals to the brain. In someone with chronic pain, these neurons send pain signals to the brain even when an injury isn’t present. A physical medicine pain specialist’s job is to determine what is causing these neurons to fire, and how to stop them from incorrectly firing.

The A11 cluster might be causing some of these neurons to fire. In fact, when removed, mice were still able to feel acute pain (an actual physical injury), but they exhibited a lesser response to chronic pain.

“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,” said Dr. Price. “This may open up new opportunities to target medicines that could reverse chronic pain,” said Dr. Price.

Dr. Price and colleagues want to continue studying dopamine receptors in relation to chronic pain perception.

“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.”

Study: Chronic Pain Linked To Activation of Brain’s Glial Cells

A new study published in Reuters Health suggests that doctors may soon have another area to target when it comes to treating chronic pain: your brain’s glial cells.

Researchers said their study indicated that patients with chronic pain often show signs of glial cell activation in areas of the brain that modulate pain.

“Glia appears to be involved in the pathophysiology of chronic pain, and therefore we should consider developing therapeutic approaches targeting glia,” said Dr. Marco L. Loggia, of Massachusetts General Hospital. “Glial activation is accompanied by many cellular responses, which include the production and release of substances (such as so-called ‘pro-inflammatory cytokines’) that can sensitize the pain pathways in the central nervous system. Thus, glial activation is not a mere reaction to a pain state but actively contributes to the establishment and/or maintenance of persistent pain.”

Brain Glial

Glial Study

To test the theory that chronic pain sufferers experience activation of brain glia, Dr. Loggia and his team analyzed data from 19 patients with chronic low back pain and 25 non-chronic pain volunteers. After analyzing translocator protein (TPSO) levels associated with the activation of brain glia, researchers found:

  • Protein increases were significantly higher in patients with chronic low back pain than in the control group.
  • There were no brain regions in which the control group experienced a higher protein presence than the chronic back pain group.

“It’s important to stress that although TSPO upregulation is a marker of glial activation and therefore of a pro-inflammatory state, animal studies suggest that its role is actually to limit the magnitude of glial responses after their initiation, thereby promoting the return to pre-injury pain-free status and recovery from pain,” said Dr. Loggia. “This means that what we are imaging may be the process of glial cells trying to ‘calm down’ after being activated by the pain. Thus, subjects with low levels of pain-related TSPO upregulation on activated glia may be less able to adequately inhibit neuroinflammatory responses, and have a more exaggerated response that ultimately leads to more inflammation and pain.”

Dr. Loggia continued:

“No objective biomarkers exist to determine if somebody is in pain (i.e. you can’t just hook someone up to a machine to see if they’re experiencing chronic pain). Thus, this study – aside from suggesting glia as a therapeutic target for pain – is important as it may provide an important step toward the identification of objective biomarkers for pain conditions.”

He concluded by saying knowledge of human glial activation had been limited, prior to the study.

“In animal studies we know that glial modulators, which limit glial activation, can potently inhibit or reverse pain,” Dr. Loggia said. “However, evidence of glial involvement in human pain has been very limited until now. Observing glial activation in humans has important potential implications for the development of new therapies based on glial modulation. Seeing that glial activation really happens in patients will provide the rationale to justify a more aggressive exploration of this therapeutic route, and identify which patients are more likely to benefit from these types of therapies.”

Related source: Reuters, Scientific American