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dc.contributor.authorTsunematsu, Tomomi
dc.contributor.authorKilduff, Thomas S.
dc.contributor.authorTakahashi, Satoru
dc.contributor.authorTominaga, Makoto
dc.contributor.authorYamanaka, Akihiro
dc.contributor.authorBoyden, Edward
dc.date.accessioned2011-09-21T22:16:05Z
dc.date.available2011-09-21T22:16:05Z
dc.date.issued2011-05
dc.date.submitted2011-04
dc.identifier.issn0270-6474
dc.identifier.issn1529-2401
dc.identifier.urihttp://hdl.handle.net/1721.1/65925
dc.description.abstractOrexin/hypocretin neurons have a crucial role in the regulation of sleep and wakefulness. To help determine how these neurons promote wakefulness, we generated transgenic mice in which orexin neurons expressed halorhodopsin (orexin/Halo mice), an orange light-activated neuronal silencer. Slice patch-clamp recordings of orexin neurons that expressed halorhodopsin demonstrated that orange light photic illumination immediately hyperpolarized membrane potential and inhibited orexin neuron discharge in proportion to illumination intensity. Acute silencing of orexin neurons in vivo during the day (the inactive period) induced synchronization of the electroencephalogram and a reduction in amplitude of the electromyogram that is characteristic of slow-wave sleep (SWS). In contrast, orexin neuron photoinhibition was ineffective during the night (active period). Acute photoinhibition of orexin neurons during the day in orexin/Halo mice also reduced discharge of neurons in an orexin terminal field, the dorsal raphe (DR) nucleus. However, serotonergic DR neurons exhibited normal discharge rates in mice lacking orexin neurons. Thus, although usually highly dependent on orexin neuronal activity, serotonergic DR neuronal activity can be regulated appropriately in the chronic absence of orexin input. Together, these results demonstrate that acute inhibition of orexin neurons results in time-of-day-dependent induction of SWS and in reduced firing rate of neurons in an efferent projection site thought to be involved in arousal state regulation. The results presented here advance our understanding of the role of orexin neurons in the regulation of sleep/wakefulness and may be relevant to the mechanisms that underlie symptom progression in narcolepsy.en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Grant R01NS057464)en_US
dc.language.isoen_US
dc.publisherSociety for Neuroscienceen_US
dc.relation.isversionofhttp://dx.doi.org/10.1523/JNEUROSCI.0784-11.2011en_US
dc.rightsArticle is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.en_US
dc.sourceMIT web domainen_US
dc.titleAcute optogenetic silencing of orexin/hypocretin neurons induces slow wave sleep in miceen_US
dc.typeArticleen_US
dc.identifier.citationTsunematsu, T. et al. “Acute Optogenetic Silencing of Orexin/Hypocretin Neurons Induces Slow-Wave Sleep in Mice.” Journal of Neuroscience 31.29 (2011) : 10529-10539. Copyright ©2011 the authorsen_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biological Engineeringen_US
dc.contributor.departmentProgram in Media Arts and Sciences (Massachusetts Institute of Technology)en_US
dc.contributor.approverBoyden, Edward Stuart
dc.contributor.mitauthorBoyden, Edward Stuart
dc.relation.journalJournal of Neuroscienceen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsTsunematsu, T.; Kilduff, T. S.; Boyden, E. S.; Takahashi, S.; Tominaga, M.; Yamanaka, A.en
dc.identifier.orcidhttps://orcid.org/0000-0002-0419-3351
mit.licensePUBLISHER_POLICYen_US
mit.metadata.statusComplete


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