Ventromedial medulla inhibitory neuron inactivation induces REM sleep without atonia and REM sleep behavior disorder

Sara Valencia Garcia, Frédéric Brischoux, Olivier Clément, Paul-Antoine Libourel, Sébastien Arthaud, Michael Lazarus, Pierre-Hervé Luppi and Patrice Fort ()
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Sara Valencia Garcia: CNRS UMR 5292, INSERM U1028
Frédéric Brischoux: CNRS UMR 5292, INSERM U1028
Olivier Clément: CNRS UMR 5292, INSERM U1028
Paul-Antoine Libourel: CNRS UMR 5292, INSERM U1028
Sébastien Arthaud: CNRS UMR 5292, INSERM U1028
Michael Lazarus: University of Tsukuba
Pierre-Hervé Luppi: CNRS UMR 5292, INSERM U1028
Patrice Fort: CNRS UMR 5292, INSERM U1028

Nature Communications, 2018, vol. 9, issue 1, 1-11

Abstract: Abstract Despite decades of research, there is a persistent debate regarding the localization of GABA/glycine neurons responsible for hyperpolarizing somatic motoneurons during paradoxical (or REM) sleep (PS), resulting in the loss of muscle tone during this sleep state. Combining complementary neuroanatomical approaches in rats, we first show that these inhibitory neurons are localized within the ventromedial medulla (vmM) rather than within the spinal cord. We then demonstrate their functional role in PS expression through local injections of adeno-associated virus carrying specific short-hairpin RNA in order to chronically impair inhibitory neurotransmission from vmM. After such selective genetic inactivation, rats display PS without atonia associated with abnormal and violent motor activity, concomitant with a small reduction of daily PS quantity. These symptoms closely mimic human REM sleep behavior disorder (RBD), a prodromal parasomnia of synucleinopathies. Our findings demonstrate the crucial role of GABA/glycine inhibitory vmM neurons in muscle atonia during PS and highlight a candidate brain region that can be susceptible to α-synuclein-dependent degeneration in RBD patients.

Date: 2018
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DOI: 10.1038/s41467-017-02761-0

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