Natural Paralysis During Sleep

EnolaGaia

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I've long known that somehow the brain disengages the body's voluntary motor control during sleep, and I've therefore long suspected that certain sleep disorders and sleep paralysis incidents involved a malfunction in this naturally dysfunctional state.

Japanese researchers have now identified neuron groups in mice that actively suppress movement during REM sleep - the phase when the brain is most active and we are dreaming.
Researchers Discover How the Brain Paralyzes You While You Sleep

Researchers at the University of Tsukuba in Japan have discovered a group of neurons in the mouse brainstem that suppress unwanted movement during rapid eye movement sleep.

... {N}arcolepsy, cataplexy, and rapid eye movement (REM) sleep behavior disorder are all serious sleep-related illnesses. Researchers at the University of Tsukuba led by Professor Takeshi Sakurai have found neurons in the brain that link all three disorders and could provide a target for treatments.

REM sleep correlates when we dream. Our eyes move back and forth, but our bodies remain still. This near-paralysis of muscles while dreaming is called REM-atonia, and is lacking in people with REM sleep behavior disorder. Instead of being still during REM sleep, muscles move around, often going as far as to stand up and jump, yell, or punch. Sakurai and his team set out to find the neurons in the brain that normally prevent this type of behavior during REM sleep.

Working with mice, the team identified a specific group of neurons as likely candidates. ... “The anatomy of the neurons we found matched what we know,” explains 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 began moving during their sleep, just like someone with REM sleep behavior disorder.

Narcolepsy, as demonstrated by Homer Simpson, is characterized by suddenly falling asleep at any time during the day, even in mid-sentence (he was diagnosed with narcolepsy). Cataplexy is a related illness in which people suddenly lose muscle tone and collapse. Although they are awake, their muscles act as if they are in REM sleep. Sakurai and his team suspected that the special neurons they found were related to these two disorders. They tested their hypothesis using 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,” says Sakurai. ...

FULL STORY: https://scitechdaily.com/researchers-discover-how-the-brain-paralyzes-you-while-you-sleep/
 

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Here are the bibliographic details and abstract from the published Japanese study ...

A discrete glycinergic neuronal population in the ventromedial medulla that induces muscle atonia during REM sleep and cataplexy in mice
Shuntaro Uchida, Shingo Soya, Yuki C. Saito, Arisa Hirano, Keisuke Koga, Makoto Tsuda, Manabu Abe, Kenji Sakimura and Takeshi Sakurai
Journal of Neuroscience 28 December 2020, JN-RM-0688-20
DOI: https://doi.org/10.1523/JNEUROSCI.0688-20.2020

Abstract
During rapid eye movement (REM) sleep, anti-gravity muscle tone and bodily movements are mostly absent, because somatic motoneurons are inhibited by descending inhibitory pathways. Recent studies showed that glycine/GABA neurons in the ventromedial medulla (VMM) (GlyVMM neurons) play an important role in generating muscle atonia during REM sleep (REM-atonia). However, how these REM-atonia-inducing neurons interconnect with other neuronal populations has been unknown. In the present study, we first identified a specific subpopulation of GlyVMM neurons that play an important role in induction of REM-atonia by virus vector-mediated tracing in male mice in which glycinergic neurons expressed Cre recombinase. We found these neurons receive direct synaptic input from neurons in several brain stem regions, including glutamatergic neurons in the sublaterodorsal tegmental nucleus (SLD) (GluSLD neurons). Silencing this circuit by specifically expressing tetanus toxin light chain (TeTNLC) resulted in REM sleep without atonia. This manipulation also caused a marked decrease in time spent in cataplexy-like episodes when applied to narcoleptic orexin-ataxin-3 mice. We also showed that GlyVMM neurons play an important role in maintenance of sleep. This present study identified a population of glycinergic neurons in the VMM that are commonly involved in REM-atonia and cataplexy.

https://www.jneurosci.org/content/early/2020/12/22/JNEUROSCI.0688-20.2020
 
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