A small Area of the Brain can shuts Down the Pain - Know How? - Seeker's Thoughts

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A small Area of the Brain can shuts Down the Pain - Know How?


A research team has found a small area of the brain in mice that can profoundly control the animals’ sense of pain. Somewhat unexpectedly, this brain center turns pain off, not on. It’s 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 response, like the fight to fight response and general anxiety.


People do believe there is a central place to relieve pain that’s why placebos work- but how?

Sometimes a person can have a response to a placebo. The response can be positive or negative. For instance, a person’s symptoms may improve. Or the person may have what appears to be side effects from the treatment. These responses are known as the placebo effect.



There are some conditions in which placebo can produce results even when people know they are taking a placebo. Studies show that placebos can have an effect on condition such as depression, pain, sleep disorders, irritable bowel syndrome, and menopause.

Research on the Placebo effect has focused on the relationship of mind and body. One of the most common theories is that the placebo effect is due to a person’s expectations. If a person expects a pill to do something, then it’s possible that the body’s own chemistry can cause effects similar to what a medication might have caused.

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Now the question is where in the brain is the center that can turn off the pain?

  Most of the previous studies have focused on which regions are turned ON by pain. But there are so many regions processing pain, you’d have to turn them all off to stop pain whereas this one center can turn off the pain by itself.


 The Fan Wang, the Morris N. Board distinguished professor of neurology in the school of medicine. 


The work is a follow up earlier research in Wang’s lab looking at neuron that are activated, rather than suppressed, by a general anesthetic. In a 2019 study, they 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 neuron (CeA stands for central amygdala; ga indicates activation by general anesthesia).

Mice have a relatively larger central amygdala than humans, however, according to Wang – there is no reason to think that we have a different system of 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, which was a surprise.

By giving mice a mild pain stimulus, the researchers could map all 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 inhibitor input form the CeAga.


According to Wang, pain is a complicated brain response. It involves sensory discrimination, emotions, 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.


What technology researchers used for this breakthrough discovery?

Using a technology called ontogenetic, 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. Par-licking or face-wiping behaviors were completely abolished” the moment the light was switched on to activate the anti center.


It was so drastic – they instantaneously stop licking and rubbing.

When the scientists dampened the activity if these CeAga neurons, the mice responded as if a temporary insult had become intense or painful again. They also found that low-dose ketamine and anesthetic drug that allows sensation but blocks pain activated the CeAga center and wouldn’t work without it.





Conclusion

Now researchers are going to look for drugs that can activate only these cells to suppress pain potential future pain killers.

The other thing is researchers are trying to do is (transcriptome) sequence the hell out of these cells. The researchers are hoping to find the gene for a rare or unique cell surface receptor among these specialized cells that would enable a very specific drug to activate these neurons and relieve pain.

Source – Duke university

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