A Discrete Glycinergic Neuronal Population in the Ventromedial Medulla That Induces Muscle Atonia during REM Sleep and Cataplexy in Mice

How neurons control sleep-associated muscle paralysis

28 October 2021

A population of neurons in the brainstem that play a critical role in promoting temporary muscle paralysis during rapid eye movement (REM) sleep has been identified.

REM sleep is the stage of slumber typically associated with dreaming and consolidation of memories, but some people suffer from REM behaviour disorder (RBD), a condition marked by action-filled dreams that disturb sleep patterns and often cause physical injury.

By tracing neural circuits in slumbering mice, a team led by University of Tsukuba researchers has shown that a subset of neurons in the ventromedial medulla of the brainstem release the inhibitory neurotransmitter glycine and interact with other neurons in the surrounding brain and spinal-cord tissues to control muscle activity.

Genetic silencing of these glycine-producing neurons caused the mice to enter REM sleep without muscle paralysis. Therapies that activate this neural circuitry might therefore help quash muscle movement in RBD sufferers.

Supported content

References

1. Journal of Neuroscience 41, 1582–1596 (2021). doi: 10.1523/JNEUROSCI.0688-20.2020