In a new study, researchers have found a small area of the brain that could profoundly control the sense of pain.
This brain center turns pain off, not on. It’s also located in an area where few people would have thought to look for an anti-pain center, the amygdala, which is often considered the home of negative emotions and responses, like the fight or flight response and general anxiety.
The study was conducted by a Duke University research team.
The work is a follow-up to earlier research in looking at neurons that are activated, rather than suppressed, by general anesthetics.
In a 2019 study, the team found that general anesthesia promotes slow-wave sleep by activating the supraoptic nucleus of the brain.
But sleep and pain are separate, an important clue that led to the new finding.
The researchers found that general anesthesia also activates a specific subset of inhibitory neurons in the central amygdala, which they have called the CeAga neurons (CeA stands for central amygdala; ga indicates activation by general anesthesia).
Mice have a relatively larger central amygdala than humans, but Wang said she had no reason to think we have a different system for controlling pain.
Using technologies to track the paths of activated neurons in mice, the team found the CeAga was connected to many different areas of the brain.
By giving mice a mild pain stimulus, the researchers could map all of the pain-activated brain regions.
They discovered that at least 16 brain centers known to process the sensory or emotional aspects of pain were receiving inhibitory input from the CeAga.
The team says pain is a complicated brain response. 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.
Using a technology called optogenetics, which uses light to activate a small population of cells in the brain, the researchers found they could turn off the self-caring behaviors a mouse exhibits when it feels uncomfortable by activating the CeAga neurons.
The team also found that low-dose ketamine, an anesthetic drug that allows sensation but blocks pain, activated the CeAga center and wouldn’t work without it.
Now the researchers are going to look for drugs that can activate only these cells to suppress pain as potential future pain killers.
The lead author of the study is Fan Wang, the Morris N. Broad Distinguished Professor of neurobiology in the School of Medicine.
The study is published in Nature Neuroscience.
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