Researchers at Duke University have found that a small group of cells in the brain may be able to regulate our sense of pain. Using mouse models, they found the cells in the amygdala.
The findings are a follow-up to earlier research investigating how neurons are activated by general anesthetics. In 2019, the same researchers found that general anesthesia promotes slow-wave sleep as it activates a specific subset of neurons in the central amygdala, known as CeAga neurons.
Using various technologies, the researchers tracked the pathways of neurons activated in mice after giving them a mild pain stimulus. In total, they found that at least 16 areas of the brain known to process sensory and emotional aspects of pain received inhibitory signals from the CeAga.
"Pain is a complicated brain response," says senior author of the study, Fan Wang said. "It involves sensory discrimination, emotion, and autonomic (involuntary nervous system) responses. Treating pain by dampening all of these brain processes in many areas is very difficult to achieve. But activating a key node that naturally sends inhibitory signals to these pain-processing regions would be more robust."
Next, the researchers used a technology known as optogenetics, that activates various parts of the brain with a ‘light’, to activate the CeAga neurons. In doing so, they found they could turn off self-caring behaviors in mice when they feel uncomfortable, such as licking their paws. Reducing the activity of these neurons caused the mice to immediately revert to comfort-seeking behaviors.
Furthermore, they found that low doses of anesthetic drug ketamine, known to allow sensation but block pain, also activated the CeAga cells, and could not function without them.
Now, the researchers intend to identify the gene responsible for this process, and thus a drug target, so may then develop treatments to relieve pain using this mechanism.