Understanding the Genetic Pathway Linking Heart and Brain in Fainting (Syncope)

What exactly is fainting? Scientists have solved the mystery by discovering a surprising connection between the heart and the brain. What it is. While almost 40% of the population experiences fainting in their lifetime, scientists have not yet known the exact mechanism when we experience this brief lack of consciousness. Now, researchers from the University of California (UC) San Diego have identified, for the first time given, the precise genetic pathway connecting the heart to the brain that triggers fainting, called syncope. The study was published in the journal Nature. This opens a path to finding effective treatments for conditions where fainting is prevalent and persistent. Traditionally, it was believed that the brain sent a signal to the heart, which quickly followed the instructions. But the team, led by assistant professor of biological sciences Vineet Augustine, was able to show that this pathway was not complete, until now. “What we’re finding is that the heart also sends signals back to the brain that can change brain function . Our study is the first comprehensive demonstration of a genetically defined cardiac reflex that faithfully recapitulates the characteristics of human syncope at the physiological, behavioral and neural levels,” said Augustine. The team analyzed the neural mechanisms related to the Bezold-Jarisch reflex (BJR), cardiac function which was identified in 1867. BJR, which presents with reduced heart rate, blood pressure and breathing, was thought to be associated with fainting, but was never proven. Researchers analyzed the genetic makeup of a sensory group known as the nodular ganglia, which is part of the vagus nerves that carry signals between the brain and the heart. Vagal sensory neurons (VSNs) send signals to the brainstem and have been linked to BJR and syncope. They found that VSNs expressing neuropeptide Y receptor Y2 (NPY2R) have a significant connection to BJR physiology. Using optogenetics to target specific neurons, the researchers were able to trigger NPY2R VSNs in mice, which caused the animals to pass out instantly. Using observational data, whole-brain neural data, and machine learning, the scientists were able to show how essential NPY2R was in triggering fainting. What’s more, when these neurons were activated, the mice experienced pupil dilation and the familiar fainting sensation. “eye rolling” seen in humans, plus slower heart rate and breathing and a drop in blood pressure. “We were amazed to see how their eyes rolled back at the same time as their brain activity dropped rapidly.” , the researchers reported in an abstract of the paper. “Then, after a few seconds, brain activity and movement returned. This was our Evrika moment!” When the NPY2R VSNs were removed, BJR and fainting in mice ceased. So while previous studies have shown how a reduction in blood flow to the brain triggers fainting, it now seems obvious that the pathway is a two-way street, with information being sent back to the brain. “People in neuroscience traditionally think that the body just follows the brain, but now it’s becoming very clear that the body sends signals to the brain and then the brain changes its function,” he Augustine said. The findings offer potential research avenues for better understanding and treatment of a range of psychiatric and neurological disorders that have a distinct brain-heart connection. The team now hopes to track the exact conditions that are required to excite VSNs and to use the research to develop targeted therapies for health conditions associated with fainting, writes doctorulzilei.ro.

Source: ReplicaOnline.ro

2023-11-08 23:44:32
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