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How the brain paralyzes the body during REM sleep

A new study from the University of Tsukuba has identified a group of neurons in the brain that restrict movement during REM sleep. This new understanding of how the brain paralyzes the body throughout REM sleep may ultimately provide a target for disorders like narcolepsy and cataplexy.

During REM sleep, our eyes move back and forth as we dream, but our bodies remain still. This protective state of temporary paralysis of the arms and legs, known as atonia, does not occur in people with REM sleep behavior disorder. 

Instead of lying still, people with REM sleep behavior disorder experience muscle movement. These individuals may stand up, jump around, and even yell or punch as they are dreaming.

The Tsukuba team set out to identify the neurons in the brain that promote atonia. Using a mouse model, the researchers found a specific group of neurons located in the ventral medial medulla that were the most likely candidates. These particular neurons receive input from another brain region called the sublaterodorsal tegmental nucleus (SLD).

“The anatomy of the neurons we found matched what we know,” explained study lead author Professor Takeshi Sakurai. “They were connected to neurons that control voluntary movements, but not those that control muscles in the eyes or internal organs. Importantly, they were inhibitory, meaning that they can prevent muscle movement when active.” 

When the researchers blocked the input to these neurons, the mice started moving during their sleep, just like someone with REM sleep behavior disorder.

People with narcolepsy can suddenly fall asleep at any time during the day, even in mid-sentence. Individuals with cataplexy suddenly lose muscle tone and collapse as if they are in a state of REM sleep when they are actually awake

Professor Sakurai and his team theorized that the special neurons they identified were related to both disorders. To investigate, the experts used a mouse model of narcolepsy in which cataplexic attacks could be triggered by chocolate. 

“We found that silencing the SLD-to-ventral medial medulla reduced the number of cataplexic bouts,” said Professor Sakurai.

The experiments revealed that these special circuits control muscle atonia in both REM sleep and cataplexy. 

“The glycinergic neurons we have identified in the ventral medial medulla could be a good target for drug therapies for people with narcolepsy, cataplexy, or REM sleep behavior disorder,” said Professor Sakurai.

“Future studies will have to examine how emotions, which are known to trigger cataplexy, can affect these neurons.”

The study is published in the Journal of Neuroscience.

By Chrissy Sexton, Staff Writer

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