If you’ve ever fainted, you might remember the sudden feeling of dizziness or nausea right before you pass out. Maybe your ears started to ring. Your vision got blurry. And just like that, you were out cold. You might’ve woken up and confusedly wondered: Why did that happen?
For years, researchers have attributed fainting, or “syncope,” to a sudden restriction in blood flow to the brain. But the mechanism behind why and how this happens has remained a mystery.
Now, in a study published this month in Nature, researchers describe a heart-brain pathway in mice that induces fainting when its neurons are activated.
“This is the first step to show there is much more to fainting than just reduced blood flow,” Vineet Augustine, a neurobiologist at the University of California, San Diego (UCSD), and one of the study’s authors, tells Aria Bendix of NBC News. “The blood flow reduction does play a role, but there are other brain circuits at play here… It is not as simple as what cardiology textbooks would say.”
To better understand syncope, the team of researchers focused their attention on mice. They studied a collection of neurons in the vagus nerve, which connects the brain to the heart and digestive system. The vagus nerve helps with a variety of bodily functions, including digestion, heart rate, coughing, sneezing, swallowing and vomiting. It also helps the body end its fight-or-flight response.
The researchers identified specific neurons within this pathway called NPY2R VSNs that link the lower chambers of the heart to the brainstem. These neurons express a receptor associated with blood vessel contractions.
Using ultrasound imaging and optogenetics—a method of controlling neurons with light—the researchers triggered the NPY2R VSNs to see what would happen, writes Miryam Naddaf for Nature News. Within a few seconds, mice that had previously been moving around lost consciousness. After a few more seconds, they began to regain consciousness and walk again.
“We honestly weren’t 100 percent sure what to expect,” Jonathan Lovelace, a neuroscientist at UCSD and a co-author of the paper, tells Science’s Robin Donovan. “But I don’t think having them fall over and faint was at the top of the list.”
Upon activation of NPY2R VSNs, the mice also showed classic signs of syncope in humans, including rapid pupil dilation, eye rolling, lower blood pressure, lower heart rates, suppressed breathing rates and reduced blood flow to the brain. More testing showed that when the researchers removed NPY2R VSNs, fainting conditions disappeared, per a statement from UCSD.
Additionally, the team discovered that when the mice were knocked unconscious, neuron activity decreased in all areas of the brain except for one: the periventricular zone, a region of the hypothalamus. When researchers blocked activity in this area, the mice took more time to regain consciousness. When they stimulated this region, the mice awoke. This suggests that syncope and recovery are somehow regulated by a network that includes both NPY2R VSNs and the periventricular zone, per Nature News.
“Coming from a clinical standpoint, this is all very exciting,” Richard Sutton, a clinical cardiologist at Imperial College London who was not involved in the study, tells the publication. The work “doesn’t answer all questions immediately… but I think it could answer, with future research, almost everything.”
By furthering understanding of the human heart, this research could be relevant for helping treat cardiovascular diseases, which are the leading cause of death around the world, write the authors in the paper.
Plus, the study could inspire new approaches for preventing fainting, which affects approximately 40 percent of people at some point in their lives. To treat syncope, doctors could replace or remove genes related to the vagus nerve, per NBC News.
“You could potentially imagine that there’ll be therapies on the horizon,” Zachary Goldberger, a cardiologist at the University of Wisconsin–Madison School of Medicine and Public Health who did not participate in the research, tells the publication.