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January 14, 2025 | Neuron
In a groundbreaking study, scientists have revealed new insights into how the brain encodes pain, shedding light on the neuronal mechanisms behind nociceptive-evoked gamma oscillations (GBOs). A team of researchers at the Institute of Psychology, Chinese Academy of Sciences, led by Prof. Hu Li, has identified a specific type of neuron in the brain’s primary somatosensory cortex (S1) that plays a critical role in processing pain intensity.
Published in the renowned journal Neuron on January 13, the study details how parvalbumin (PV) interneurons in the S1 cortex are key players in encoding pain. These neurons not only respond to painful stimuli but also drive GBOs—brain waves linked to pain perception. This discovery could pave the way for new therapeutic strategies targeting these oscillations to manage chronic pain more effectively.
Pain is one of the most pervasive sources of human suffering, affecting millions worldwide and causing a significant economic burden. Despite its impact, pain remains notoriously difficult to treat due to its subjective nature, making accurate diagnosis and tailored therapies challenging. Researchers have long sought neural biomarkers that can objectively measure and assess pain, with GBOs emerging as a promising candidate.
The new study builds on previous research showing that GBOs are reliable indicators of pain-related behaviors in both humans and animals. However, the exact neural mechanisms behind these oscillations had remained elusive—until now. Through a combination of high-density EEG, silicon probes, calcium imaging, and optogenetics, the research team was able to pinpoint PV interneurons as the source of the oscillations’ role in encoding pain.
The results show that PV interneurons, rather than other types of neurons like pyramidal cells, preferentially track pain intensity. These findings were confirmed across species, including humans and rodents, reinforcing the idea that PV interneurons in S1 are essential to the brain’s pain processing. Importantly, the researchers demonstrated that altering PV interneuron activity—either through activation or inhibition—can modify pain-related behaviors, as well as the GBOs themselves.
“The discovery that PV interneurons are responsible for the selective encoding of pain intensity has profound implications not only for our understanding of pain perception but also for clinical applications,” said Prof. Hu. “With GBOs now recognized as potential biomarkers for pain, this research opens up exciting possibilities for pain management and drug development.”
As the study illuminates the precise brain circuits involved in pain processing, it could lead to more effective treatments for a range of pain disorders. Given the increasing recognition of GBOs as reliable markers of pain, the study’s findings hold promise for advancing both pain diagnostics and therapeutic approaches in clinical practice.
For further reading, the full study, titled “Neuronal Mechanisms of Nociceptive-Evoked Gamma-Band Oscillations in Rodents,” can be accessed in Neuron (DOI: 10.1016/j.neuron.2024.12.011).
