40% of people faint at least once in their life. But what causes fainting or the sudden and momentary loss of consciousness due to a change in brain function? And we're not referring to triggers like hunger, heat, fatigue or fear, but the very physiological mechanism that turns off and luckily turns on the switch: well, a study just published in Nature may have finally identified it.
One of the known causes of fainting is the so-called Bezold-Jarisch reflex, the combination of three symptoms (bradycardia, low blood pressure and slow breathing rate) caused by momentary dysfunction of the vagus nerve, a cranial nerve that connects the brain with the heart, digestive system and lungs. A group of neuroscientists from the University of California, San Diego has now discovered a neural circuit in mice that connects the heart and the brain and that may underlie this reflex.
Using genetic analysis and fluorescent tracing techniques, scientists have identified a special group of sensory nerve cells in the vagus nerve called NPY2R.
This population of neurons connects the cardiac ventricles to a small region of the brainstem (the structure located at the base of the brain and connected to the spinal cord), called the zona postrema. There is also a receptor on neurons NPY2R that plays a role in the constriction of blood vessels.
At this point the researchers used optogenetics, a technique that allows you to control neural activity through light, to stimulate the newly discovered neurons in some mice while monitoring their heart rate, blood pressure and eye movements. They would never expect the animals to respond to the activation of NPY2R neurons with the typical symptoms of syncope: drop in heart rate and breathing rate, drop in blood pressure, dilated pupils and backward looking eyes. In short, complete fainting, lasting 7-8 seconds.
When this neural circuit was blocked, the mice no longer fainted with the same stimulation. The team also performed a series of other tests to show that there was no overlap between this and other circuits, ie. that other nerve cells that can influence blood vessels did not have the same effect, and at the same time, NPY2R neurons did not receive external input from other organs.
It was the vasoconstrictor power of receptors on NPY2R cells that reduces blood flow to the brain and forces the typical blackout to stop. It remains to be elucidated why, just before syncope, these neurons are stimulated. The nervous system, which controls involuntary body functions that were not considered in the study, may have a role.
The team eventually found that during periods of fainting, the mice's brain activity decreased everywhere except in a small part of the hypothalamus, an important central nervous system structure located in the central area within the two cerebral hemispheres. When the scientists inhibited the activity of this area, the mice's periods of fainting lasted longer, and when they stimulated it, the animals recovered. Therefore, this region would be involved in rapid awakenings from fainting, which allow the correct flow of oxygen and glucose to be restored to the brain.
From a clinical point of view, what has been discovered can be used to study pharmacological strategies to limit fainting in those who are particularly prone to these episodes. (A2 Televizion)
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