End of the mystery: Why do we all get tired at the end of the day?
Have you always wondered why after a long day it is simply impossible to keep your eyes open? A new study has identified groups of cells in the brain that measure the time we are awake - creating pressure - and forcing us to sleep. The researchers: "May reveal ways to provide resistance to sleep deprivation and other physiological challenges."
We all know that feeling after a long day of work - we want to watch a series, a movie, or a live game - but the feeling of fatigue overcomes us and forces us to go to bed. This phenomenon is called by scientists "sleep drive". For years, researchers have been trying to understand how the brain tracks the time we spend awake and translates it into the physical need to close our eyes. Now, researchers from the University of Basel in Switzerland claim they have managed to crack the mechanism.
The new study, published in the prestigious scientific journal Nature, was conducted in collaboration with researchers from the Beth Israel Deaconess Medical Center in Boston and Auburn University. As part of the study, the scientists managed to identify specific neurons in the brain of mice, which are activated during prolonged wakefulness and play a crucial role in creating the feeling of fatigue.
"We identified populations of neurons that monitor prolonged wakefulness and actively promote sleep," explained the head of the research team, Prof. Alex Schier from the Biozentrum at the University of Basel. "This is a missing and important piece of the puzzle that explains why we become tired."
Not just reacting - but creating the drive to sleep
To identify the areas involved in the brain, the researchers compared brain activity patterns in mice during normal sleep and wake cycles, during sleep deprivation, and during recovery sleep.
The computer analysis revealed certain areas that reflected the length of time the animals were awake. Within one of these areas, two separate neuron populations were located in the brainstem. The activity of these populations increased as the animals remained awake longer, and dropped again with the transition to sleep. To test whether the cells just "report" fatigue or actually cause it, the researchers activated them artificially.
The result: the mice slept longer and deeper, similar to the recovery sleep that occurs after sleep deprivation. Conversely, when the researchers inhibited the activity of these cells, the mice's sleep decreased and they remained alert. "These neurons do not simply signal that an animal has been awake," emphasizes Prof. Schier. "Our experiments show that they are essential for promoting sleep, and that they may be key components of the neural network that generates the sleep drive."
The unexpected result: little sleep without severe damage
One of the most surprising findings in the study was recorded when the researchers inhibited these two neuron populations in the long term. As a result, the mice's need for sleep dropped sharply - and they slept about 70% less than usual.
Unexpectedly, most of these mice did not suffer from severe behavioral impairments that almost always accompany such a severe lack of sleep. According to the researchers, this finding indicated that these cells determine not only how much we will sleep, but also how strongly the pressure to go to sleep will build up over time.
According to Dr. William Jo, the first author of the study, the new insights may open completely new horizons for sleep research: "Future studies could reveal how the neurons we identified interact with the rest of the brain, and how the sleep drive is generated at the molecular level. Our ability to stably alter sleep behavior will allow us to investigate adaptation to long-term sleep loss - which may in the future reveal ways to provide resistance to sleep deprivation and other physiological challenges."
