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dc.contributor.author
Ma, Ying
dc.contributor.author
Miracca, Giulia
dc.contributor.author
Yu, Xiao
dc.contributor.author
Harding, Edward C.
dc.contributor.author
Miao, Andawei
dc.contributor.author
Yustos, Raquel
dc.contributor.author
Vyssotski, Alexei L.
dc.contributor.author
Franks, Nicholas P.
dc.contributor.author
Wisden, William
dc.date.accessioned
2019-10-14T12:23:14Z
dc.date.available
2019-10-08T02:42:52Z
dc.date.available
2019-10-08T09:12:42Z
dc.date.available
2019-10-14T12:23:14Z
dc.date.issued
2019-10
dc.identifier.issn
0960-9822
dc.identifier.issn
1879-0445
dc.identifier.other
10.1016/j.cub.2019.07.087
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/368947
dc.identifier.doi
10.3929/ethz-b-000368947
dc.description.abstract
Our urge to sleep increases with time spent awake, until sleep becomes inescapable. The sleep following sleep deprivation is longer and deeper, with an increased power of delta (0.5–4 Hz) oscillations, a phenomenon termed sleep homeostasis [1, 2, 3, 4]. Although widely expressed genes regulate sleep homeostasis [1, 4, 5, 6, 7, 8, 9, 10] and the process is tracked by somnogens and phosphorylation [1, 3, 7, 11, 12, 13, 14], at the circuit level sleep homeostasis has remained mysterious. Previously, we found that sedation induced with α2-adrenergic agonists (e.g., dexmedetomidine) and sleep homeostasis both depend on the preoptic (PO) hypothalamus [15, 16]. Dexmedetomidine, increasingly used for long-term sedation in intensive care units [17], induces a non-rapid-eye-movement (NREM)-like sleep but with undesirable hypothermia [18, 19]. Within the PO, various neuronal subtypes (e.g., GABA/galanin and glutamate/NOS1) induce NREM sleep [20, 21, 22] and concomitant body cooling [21, 22]. This could be because NREM sleep’s restorative effects depend on lower body temperature [23, 24]. Here, we show that mice with lesioned PO galanin neurons have reduced sleep homeostasis: in the recovery sleep following sleep deprivation there is a diminished increase in delta power, and the mice catch up little on lost sleep. Furthermore, dexmedetomidine cannot induce high-power delta oscillations or sustained hypothermia. Some hours after dexmedetomidine administration to wild-type mice there is a rebound in delta power when they enter normal NREM sleep, reminiscent of emergence from torpor. This delta rebound is reduced in mice lacking PO galanin neurons. Thus, sleep homeostasis and dexmedetomidine-induced sedation require PO galanin neurons and likely share common mechanisms.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Cell Press
en_US
dc.rights.uri
http://creativecommons.org/licenses/by/4.0/
dc.subject
Sleep homeostasis
en_US
dc.subject
Dexmedetomidine
en_US
dc.subject
Galanin
en_US
dc.subject
Body temperature
en_US
dc.subject
Preoptic hypothalamus
en_US
dc.subject
Sedation
en_US
dc.subject
NREM
en_US
dc.subject
Torpor
en_US
dc.title
Galanin Neurons Unite Sleep Homeostasis and α2-Adrenergic Sedation
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution 4.0 International
dc.date.published
2019-09-19
ethz.journal.title
Current Biology
ethz.journal.volume
29
en_US
ethz.journal.issue
19
en_US
ethz.journal.abbreviated
Curr Biol
ethz.pages.start
3315
en_US
ethz.pages.end
3322.e3
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.wos
ethz.identifier.scopus
ethz.publication.place
Cambridge, MA
en_US
ethz.publication.status
published
en_US
ethz.date.deposited
2019-10-08T02:42:56Z
ethz.source
SCOPUS
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2019-10-14T12:23:27Z
ethz.rosetta.lastUpdated
2020-02-15T22:02:31Z
ethz.rosetta.versionExported
true
ethz.COinS
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