What happens when you faint? Until very recently, the scientific answer to that was, “We’re not totally 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 that’s responsible for fainting.

Fainting – or, to use the more science-y term, syncope – is pretty common. Around 40 percent of us will experience it at least once in our lives, and it can be a response to lots of different situations: overheating; the sight of blood or needles; and even a particularly difficult poop, to name but a few. 

The usual viewpoint among neuroscientists has been that during an episode of syncope, the brain sends out signals to the heart and the heart reacts accordingly. Where this new study differs is that the researchers started thinking of the heart as its own sensory organ, and hypothesized that this communication could work both ways.

“What we are finding is that the heart also sends signals back to the brain, which can change brain function,” said senior author Vineet Augustine, an assistant professor in the University of California San Diego School of Biological Sciences, in a statement.

The team turned to some very old science to guide their research. Way back in 1867, the Bezold-Jarisch reflex (BJR), a cardiac reflex thought to be associated with fainting, was first described. It is associated with three classical symptoms that anyone who has fainted before will probably recognize: decreases in heart rate, breathing rate, and blood pressure. Even though scientists had known about the BJR for more than 150 years, there was still a lot to learn about the neural pathways underlying it.

The research zoned in on a specific type of nerve cell called vagal sensory neurons (VSNs) in the heart. VSNs are part of clusters called the nodose ganglia, themselves part of the vagus nerve, current darling of the wellness world. 

Experiments in mice showed that a subset of VSNs that express a protein called neuropeptide Y receptor Y2 (NPY2R) have a key role in the fainting response. When the scientists stimulated these VSNs themselves using optogenetics, mice that had been happily pottering about in their cages suddenly passed out. 

Just like humans, their eyes rolled into the backs of their heads and their pupils dilated. All of the characteristic signs of the BJR were there: a drop in heart rate (as you can see in the video below), slower breathing, and tanking blood pressure. Recordings taken from within thousands of neurons in the brains of the 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 around the same time as their brain activity rapidly dropped. Then, after a few seconds, brain activity and movement returned. This was our eureka moment, suggesting that we might have found neurons that can trigger syncope.”

Their suspicions were confirmed when removing those specific VSNs eliminated the fainting response. The researchers hope that this breakthrough will now lead to even deeper research, and hopefully targeted treatments for conditions that cause fainting.

Neuroscientists have long thought that the brain is the driver of fainting; but now that scientists have discovered this new and important role for the heart as well, it’s clear that both cardiac and neurological specialists are going to have work together if we’re ever truly to unravel the mystery of syncope.

The study is published in Nature.