What is it about?
Chronic pain changes how the brain and body process touch and temperature perception, often making people more sensitive. This study shows that chronic pain weakens a specific type of brain inhibitory cell in the prefrontal cortex—called parvalbumin interneuron—that normally helps reduce pain signals. These neurons rely on dopamine to function properly, but chronic pain reduces dopamine release in the prefrontal cortex. Interestingly, hunger naturally increases dopamine release and restores the ability of these cells to quiet pain circuits.
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Why is it important?
This research provides novel insights in how dopamine and pain perception are linked. By identifying how dopamine boosts the activity of specific pain-relieving neurons, it opens the door for new treatments that could target this specific pathway—providing non-opioid options for managing chronic pain.
Perspectives
This article represents nearly ten years of research, and it's rewarding to see it published in a prestigious journal. I hope the work resonates beyond the lab and encourages people to think about how behaviors like eating and somatosensory responses are all connected through the brain's chemistry. Maybe it will even spark new ideas on how we can manage pain in daily life.
Philippe Séguéla
McGill University
Read the Original
This page is a summary of: Synergistic deficits in parvalbumin interneurons and dopamine signaling drive ACC dysfunction in chronic pain, Proceedings of the National Academy of Sciences, June 2025, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2502558122.
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