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We might finally understand what happens when we pass out

What happens when you pass out? Until recently, the scientific answer to this question was: “We’re not entirely sure.” A new study has shed some light on this mystery by identifying, for the first time, the genetic pathway between the brain and heart responsible for fainting.

Fainting – or, to use the more scientific term, syncope – is quite common. About 40% of us will experience it at least once in our lives, and it can be a response to many different situations: overheating; the sight of blood or needles; and even a particularly difficult poop, to name a few.

The usual view among neuroscientists is that during an episode of syncope, the brain sends signals to the heart and the heart responds accordingly. The difference with this new study is that researchers began to view the heart as its own sensory organ and hypothesized that this communication might work both ways.

“What we find is that the heart also sends signals back to the brain, which can change how the brain functions,” said lead author Vineet Augustine, an assistant professor in the School of Biological Sciences at the University of California, San Diego, in a press release.

The team looked to very old science to guide their research. In 1867, the Bezold-Jarisch reflex (BJR), a cardiac reflex thought to be associated with fainting, was first described. It is associated with three classic symptoms that anyone who has ever lost consciousness will likely recognize: a decrease in heart rate, respiratory rate, and blood pressure. Even though scientists have known about BJR for more than 150 years, there was still much to learn about the neural pathways underlying it.

The research focused on a specific type of nerve cell called vagal sensory neurons (VSN) in the heart. The VSNs are part of groups called nodose ganglia, which in turn are part of the vagus nerve, the current darling of the wellness world.

The vagal sensory nerves of the heart are shown here in white.

Image credit: Augustine Lab, UC San Diego

Experiments in mice have shown that a subset of VSNs expressing a protein called neuropeptide Y receptor Y2 (NPY2R) plays a key role in the fainting response. When the scientists themselves stimulated these VSNs using optogenetics, mice that were happily playing in their cages suddenly fainted.

Just like humans, their eyes rolled into the back of their heads and their pupils dilated. All the characteristic signs of BJR were present: a drop in heart rate (as you can see in the video below), slower breathing and falling blood pressure. Recordings made from thousands of neurons in the brains of mice showed how blood flow and brain activity rapidly decreased.

In a summary of the work published alongside the paper, Augustine and first author Jonathan W. Lovelace said: “We were blown away when we saw how their eyes rolled back at the same time as their brain activity rapidly decreased. Then, after a few seconds, brain activity and movement returned. This was our eureka moment, suggesting that we might have found neurons capable of triggering syncope.

Their suspicions were confirmed when removing these specific VSNs eliminated the fainting response. Researchers hope this breakthrough will now lead to even more in-depth research and, hopefully, targeted treatments for conditions causing fainting.

Neuroscientists have long believed that the brain is the cause of fainting; But now that scientists have discovered this important new role of the heart, it is clear that specialists in cardiology and neurology will need to work together if we are ever to truly unravel the mystery of syncope.

The study is published in Nature.

Gn Health

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