Scientists Discover Brain Region That Tracks and Regulates Sleep Debt
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Recent research led by Mark Wu , Professor of Neurology at John Hopkins University, has potentially identified the area in mice brains responsible for tracking sleep debt and triggering restorative sleep . The study, published recently, pinpointed the thalamic nucleus as a key region involved in calculating sleep debt and inducing sleepiness, potentially paving the way for new treatments for sleep disorders if similar pathways are found in humans. Researchers used tracers and chemogenetics to identify and stimulate specific brain regions in mice, observing the effects on their sleep patterns.
The concept of sleep debt, the difference between needed and actual sleep, is familiar to many. The question of how the brain tracks and calculates this debt has remained a mystery. Mark Wu and his colleagues at John Hopkins University may have found an answer.
Wu's research discovered neurons in mice brains that tracked sleep and aided recovery from sleep debt. The next step is to determine if a similar neurological pathway exists in humans. If so, this research could be groundbreaking in developing treatments for sleep disorders and related conditions like narcolepsy.
The researchers injected mice with tracers into eleven brain regions known to induce sleep. These tracers traveled from neurons receiving signals to their source. This indicated the presence of 22 additional brain regions connected to at least four sleep-promoting areas.
The study focused on the eleven previously unidentified regions of the mice's brains. The mice were divided into eleven groups, each with three to four mice. Chemogenetics was used to inject the mice with a drug that activated a specific brain region, different for each group.
After analyzing the results, the researchers discovered the thalamic nucleus. Neuron stimulation in this area resulted in the greatest increase in non-rapid eye movement (REM) sleep in mice. The increase was almost double compared to non-stimulated time.
However, it took the mice longer to fall asleep after neuron stimulation. They seemed to be preparing to rest.
“When you go to bed, you probably brush your teeth, you wash your face, you fluff your pillow or arrange your blanket and then go to sleep. Mice do something similar. They kind of groom their face, they clean their whiskers and then they fluff their nest up,” Wu was quoted as saying by New Scientist.
This suggests that these neurons induce sleepiness rather than triggering instant sleep.
A secondary test supported this idea. Researchers deactivated brain cells in the thalamic nucleus of six sleep-deprived mice. This reduced their sleepiness, as they showed more activity and spent less time nesting compared to a control group.
These six mice also got an average of 10% less non-REM sleep. Studies also showed that these neurons automatically activated when a mouse was sleep-deprived. Their activity subsequently eased once it fell asleep.
According to Wu, these findings indicate that the thalamic nucleus induces sleepiness, tracks sleep debt, and triggers restorative sleep to pay back the debt.
However, William Giardino, Assistant Professor of Psychiatry and Behavioral Sciences at Stamford, emphasized that the existence of a similar brain circuit in humans has not been established yet. Wu's research also has not studied long-term effects.
The concept of sleep debt, the difference between needed and actual sleep, is familiar to many. The question of how the brain tracks and calculates this debt has remained a mystery. Mark Wu and his colleagues at John Hopkins University may have found an answer.
Wu's research discovered neurons in mice brains that tracked sleep and aided recovery from sleep debt. The next step is to determine if a similar neurological pathway exists in humans. If so, this research could be groundbreaking in developing treatments for sleep disorders and related conditions like narcolepsy.
The researchers injected mice with tracers into eleven brain regions known to induce sleep. These tracers traveled from neurons receiving signals to their source. This indicated the presence of 22 additional brain regions connected to at least four sleep-promoting areas.
The study focused on the eleven previously unidentified regions of the mice's brains. The mice were divided into eleven groups, each with three to four mice. Chemogenetics was used to inject the mice with a drug that activated a specific brain region, different for each group.
After analyzing the results, the researchers discovered the thalamic nucleus. Neuron stimulation in this area resulted in the greatest increase in non-rapid eye movement (REM) sleep in mice. The increase was almost double compared to non-stimulated time.
However, it took the mice longer to fall asleep after neuron stimulation. They seemed to be preparing to rest.
“When you go to bed, you probably brush your teeth, you wash your face, you fluff your pillow or arrange your blanket and then go to sleep. Mice do something similar. They kind of groom their face, they clean their whiskers and then they fluff their nest up,” Wu was quoted as saying by New Scientist.
This suggests that these neurons induce sleepiness rather than triggering instant sleep.
A secondary test supported this idea. Researchers deactivated brain cells in the thalamic nucleus of six sleep-deprived mice. This reduced their sleepiness, as they showed more activity and spent less time nesting compared to a control group.
These six mice also got an average of 10% less non-REM sleep. Studies also showed that these neurons automatically activated when a mouse was sleep-deprived. Their activity subsequently eased once it fell asleep.
According to Wu, these findings indicate that the thalamic nucleus induces sleepiness, tracks sleep debt, and triggers restorative sleep to pay back the debt.
However, William Giardino, Assistant Professor of Psychiatry and Behavioral Sciences at Stamford, emphasized that the existence of a similar brain circuit in humans has not been established yet. Wu's research also has not studied long-term effects.
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