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

Neurons that regulate sleep stages Just what sleep is for remains a bit of a mystery. During sleep, we switch several times between so-called rapid eye movement (REM) and non-REM sleep. Hayashi et al. used sophisticated developmental cell fate mapping to look at the neurons involved in the two types of sleep in mice (see the Perspective by Vyazovskiy). They identified a genetically marked population of neurons that promote non-REM sleep at the expense of REM sleep. Science, this issue p. 957; see also p. 909 The combination of neurodevelopmental techniques and chemogenetics provides insights into the brain circuitry and function of REM sleep. [Also see Perspective by Vyazovskiy] 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.