Neurosciences
Although it usually lasts no more than a minute, it is an experience experienced by about half of the people.
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It is as wide as the sea. And as yet unexplored: the brain. Although we know more and more about the mechanisms that govern it, there are still some inexplicable enigmas. And one of them is the mechanism behind the weakness. Whether from heat, hunger, standing for a long time, or just from the sight of blood or needles, 40% of people have fainted at least once in their lives. But the exact cause of this brief loss of consciousness, which experts call “syncope,” has long been a mystery to cardiologists and neuroscientists.
Now, researchers have discovered a neural pathway involving a previously undiscovered group of sensory neurons that connect the heart to the brainstem. The study, published in Nature, showed that the activation of these neurons caused the mice to become immobile almost immediately while exhibiting symptoms such as rapid pupil dilation and the classic eye movements seen during human syncope.
The mechanisms that control how and why people faint have long puzzled scientists, in part because researchers have focused on studying the heart or brain alone. But the study authors developed new tools to show how the two systems interact.
Using a cell RNA sequencing analysis of the nodose ganglia, an area of the vagus nerve (which connects the brain to many organs, including the heart), a team led by Vineet Augustine, identified a group of sensory neurons that express a type of receptor that is involved in the contraction of small muscles inside the blood vessels that cause them to contract.
The authors suggest that this neural pathway is the key to understanding fainting, beyond the observation that it is the result of reduced blood flow to the brain. “There is a reduction in blood flow, but at the same time there are specific circuits that manipulate it – explains Augustine, in a statement -.
The neurons involved, called VSN NPY2R, are different from other branches of the vagus nerve that connect to the lungs or gut. It forms branches within the lower muscular parts of the heart, the ventricles, and connects to another part of the brain stem called the area postrema.
Using a new technique that combines high-resolution ultrasound imaging with optogenetics (a method of controlling neuronal activity using light), Augustine’s team stimulated VSN NPY2R neurons in mice while monitoring the their heart rate, blood pressure, breathing, and movements. eyepieces. This method allows the team to manipulate specific neurons and visualize the heart in real time. Thanks to this, they saw the moment when the neurons were activated and it coincided with the fainting of the mice.
“We now know that there are receptors in the heart that, when activated, turn it off – concludes Jan Gert van Dijk -. Neurons in the brain are like very damaged children. They need oxygen and sugar, and they need it. now and they stop moving immediately if they fail.” Literally: these nerve cells begin to die after about 2 to 5 minutes without oxygen, but syncope usually lasts only 20 to 40 seconds. work, and they do it quickly.
For the authors, the next challenge is to study how these neurons are activated, because “this is one of the biggest enigmas of my entire career,” Augustine said.
