Oct 24, 2015

Cells of a common developmental origin regulate REM/non-REM sleep and wakefulness in mice

Science
Yu HayashiShigeyoshi Itohara

Abstract

Mammalian sleep comprises rapid eye movement (REM) sleep and non-REM (NREM) sleep. To functionally isolate from the complex mixture of neurons populating the brainstem pons those involved in switching between REM and NREM sleep, we chemogenetically manipulated neurons of a specific embryonic cell lineage in mice. We identified excitatory glutamatergic neurons that inhibit REM sleep and promote NREM sleep. These neurons shared a common developmental origin with neurons promoting wakefulness; both derived from a pool of proneural hindbrain cells expressing Atoh1 at embryonic day 10.5. We also identified inhibitory γ-aminobutyric acid-releasing neurons that act downstream to inhibit REM sleep. Artificial reduction or prolongation of REM sleep in turn affected slow-wave activity during subsequent NREM sleep, implicating REM sleep in the regulation of NREM sleep.

Mentioned in this Paper

Embryo
Entire Brainstem
ATOH1 protein, human
REM1
Regulation of Biological Process
Sleep, Slow-Wave
Neurons
Atoh1
Hindbrain
Gammalon

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