image: REM sleep, the major source of dreams, and slow wave sleep are unique to mammals and birds. view more
Credit: [Credit: Yu Hayashi]
A new study pinpoints the neurons that kick the brain out of REM sleep mode. During sleep, mammals cycle several times between different stages, called rapid eye movement (REM) and non-REM sleep. While there is some knowledge about what induces REM sleep, much less is known about what inhibits it and induces non-REM sleep. Some evidence hints that the "switch" mechanism lies in a part of the brain called the pontine tegmentum (PT). To pinpoint which neurons in this region are acting as the switch, Yu Hayashi and colleagues looked at the brain development of mouse embryos, where certain excitatory neurons migrate to the PT between day 10 and 12 of development. During this time, these neurons express a transcription factor gene called Atoh1. Using a virus that targets Atoh1, the researchers delivered a specialized receptor, hM3Dq, to only Atoh1-expressing neurons. The specialized receptor is only activated in the presence of its pharmaceutical counterpart, allowing the researchers to turn these neurons "on" at will. A series of experiments revealed that Atoh1-medial cells play a key role in regulating the sleep stages, where activation of these neurons caused a reduction in REM and an increase in non-REM sleep. Using this same technique, the team was able to identify additional neurons that inhibit non-REM in the deep mesencephalic nucleus, an area of the brain known to harbor such inhibitory neurons - although the exact type was previously unknown. Using these two types of neurons to manipulate REM sleep, Hayashi et al. also noted changes in the deep sleep patterns that occur during non-REM, hinting at a much more intricate relationship between the two stages of sleep than previously thought.
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Article #13: "Cells of a common developmental origin regulate REM/non-REM sleep and wakefulness in mice," by Y. Hayashi; M. Kashiwagi; M. Kanuka at University of Tsukuba in Tsukuba, Japan; Y. Hayashi at Japan Science and Technology Agency (JST) in Saitama, Japan; K. Yasuda; R. Ando; S. Itohara at RIKEN in Saitama, Japan; K. Sakai at Lyon Neuroscience Research Center in Lyon, France; K. Sakai at INSERM in Lyon, France; K. Sakai at CNRS in Lyon, France; K. Sakai at Claude Bernard University Lyon in Lyon, France.
Journal
Science