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A Particular Medullary-Spinal Inhibitory Pathway is Recruited for the Expression of Muscle Atonia During REM Sleep

Sara Valencia Garcia1, Pierre-Hervé Luppi1, Patrice Fort1

  • 1SLEEP Team, CNRS UMR 5292, INSERM U1028, Centre de Recherche en Neurosciences de Lyon (CRNL), Université Claude Bernard Lyon 1, Lyon, France.

Journal of Experimental Neuroscience
|November 20, 2018
PubMed

Insights

REM sleep behavior disorder (RBD) involves loss of muscle paralysis during REM sleep. Research shows dysfunction in specific brainstem neurons causes this atonia, potentially linking RBD to synucleinopathies like Parkinson's disease.

Area of Science:

  • Neuroscience
  • Sleep Medicine
  • Neurology

Background:

  • Muscle atonia is a key feature of REM sleep (paradoxical sleep), crucial for preventing dream enactment.
  • REM sleep behavior disorder (RBD) is characterized by the loss of muscle atonia during REM sleep, leading to abnormal movements.
  • RBD is a significant predictor of future synucleinopathies, particularly Parkinson's disease, with a 10-15 year latency.

Purpose of the Study:

  • To investigate the brainstem neural networks responsible for REM sleep atonia.
  • To elucidate the mechanisms underlying the loss of atonia in REM sleep behavior disorder (RBD).
  • To explore the potential link between RBD pathophysiology and synucleinopathies.

Main Methods:

  • Experiments were conducted in rats to identify and manipulate specific neuronal populations in the brainstem.
  • Utilized genetic inactivation techniques to study the role of ventromedial medullary (vmM) inhibitory neurons in REM sleep atonia.
  • Monitored locomotion and atonia during REM sleep and waking states following neuronal manipulation.

Main Results:

  • Identified pontine glutamate neurons projecting to the ventromedial medulla (vmM) during REM sleep.
  • Demonstrated that vmM inhibitory neurons (GABA/glycine) activated during REM sleep project to spinal motoneurons.
  • Genetic inactivation of vmM inhibitory neurons abolished REM sleep atonia, recapitulated RBD symptoms, and did not affect waking locomotion.

Conclusions:

  • The study identifies specific vmM inhibitory neurons as critical for generating REM sleep atonia.
  • Dysfunction or degeneration of these atonia-generating neurons may underlie REM sleep behavior disorder (RBD).
  • These findings suggest RBD could be an early manifestation of a synucleinopathic process targeting these specific neuronal populations.
Keywords:
BrainstemGABAREM sleep behavior disorderglycinepolysomnographyrat

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