Researchers have identified mouse neurons that assist the brain in managing and recovering from sleep debt. Similar pathways exist in humans and could enhance treatments for conditions associated with sleep disorders, including Alzheimer’s disease.

Everyone knows the struggle of sleep debt — the difference between the sleep one needs and what one gets. However, the mechanisms through which the brain tracks sleep loss have remained largely unclear.

Mark Woo from Johns Hopkins University and his team investigated the brain pathways of mice associated with sleep by injecting tracers into 11 brain regions known to promote sleep. The tracers revealed connections to 22 regions linked to four sleep-promoting areas.

Previous studies concentrated on a limited number of unidentified regions. A method known as chemogenetics was utilized, administering specialized drugs to the mice that activated particular areas of the brain. The mice were divided into 11 groups of 3-4 and different regions were stimulated in each group.

Interestingly, an area called the thalamic nuclear reuniens proved to be significant. Stimulation of neurons in this region resulted in a substantial increase in REM sleep for the mice — about twice as much as non-stimulated counterparts. However, it took a few hours for the stimulated mice to fall asleep, during which they exhibited signs of readiness to rest.

“When you go to sleep, you likely engage in routines like brushing your teeth, washing your face, or fluffing your pillow. Mice do something similar; they groom themselves and prepare their nests,” says Wu. This suggests that these neurons are not simple on/off switches for sleep but rather promote drowsiness.

Support for this theory came from another experiment where deactivating thalamic nuclear cells in six sleep-deprived mice resulted in decreased drowsiness. These mice were more active and nested less than the control group, averaging 10% less non-REM sleep.

Additional tests have indicated that these neurons activate during sleep deprivation and become silent when sleep begins.

Collectively, these findings indicate that this brain region not only triggers sleepiness but also facilitates recovery sleep following sleep loss, according to Wu. Targeting these neurons could lead to new therapies for sleep disorders characterized by excessive drowsiness after rest, as well as conditions like Alzheimer’s disease, where individuals struggle with sleep.

However, it’s uncertain if equivalent brain circuits exist in humans. William Gialdino from Stanford University expresses caution, stating that while the immediate effects of sleep deprivation are being studied, the long-term consequences may differ significantly from those observed in humans experiencing chronic sleep loss.