Your brain tracks your sleep debt – and now we may know how

The researchers discovered neurons in mice that help their brain to follow and recover from sleep debt. If a similar route exists in humans, it could improve treatments for sleep disorders and other conditions marked by sleep disorders, such as Alzheimer’s disease.

We all know the sleep debt, or the gap between the sleep you need and the amount you get. But so far, it was not clear how the brain follows the loss of sleep – or forces us to invent this difference.

Mark Wu at Johns Hopkins University in Maryland and his colleagues have mapped the brain in mice involved in sleep by injecting a tracer in 11 brain areas known to induce sleep. The tracer, which moves from neurons receiving signals to those who send them, revealed 22 regions with connections to at least four areas promoting sleep.

Researchers focused on a subset of 11 unidentified regions previously. Using a technique called chemiogenetics, they gave mice specialized drugs that activate special parts of their brain. They divided the mice into 11 groups of three to four individuals, activating a different area in each group.

A region called the Punionens thalamic nucleus seemed to be the key. When neurons in this area have been stimulated, mice experienced the greatest increase in the sleep of non -fast eyes (REM) – about double quantity as mice that have not been stimulated. However, animals took several hours to fall asleep after stimulation, during which they seemed to prepare for rest.

“When you go to bed, you probably brush your teeth, you wash your face, you plush your pillow or organize your blanket, then you fall asleep,” says Wu. The mice do something similar. “They somehow maintain their faces, they clean their mustaches, then they make fun of their nest,” he said. This suggests that these neurons are not a sleep switch on and out – they rather induce drowsiness.

Another test also supported this idea. In six private sleep mice, deactivation of brain cells in the thalamic nucleus made rodents less sleepy – they were more active and spent less time nesting than witness mice. They also obtained 10% less sleep not rem, on average.

Other experiences have shown that these neurons are active during sleep deprivation and calm down once sleep begins.

Together, the results suggest that this region of the brain leads to drowsiness and triggers restorative sleep after loss of sleep, explains WU. The development of therapies that target these neurons could lead to new treatments for hypersomnia – a sleep disorder characterized by excessive drowsiness after rest – as well as conditions such as Alzheimer’s disease, in which people do not sleep enough.

However, it is not clear if the same brain circuit exists in humans, explains William Gidino at the University of Stanford in California. Nor do we know if it plays a role in long -term sleep deprivation. “They focus more on the short-term effects of sleep deprivation, which may not model humans closely with years and years and years at night,” he said.