Breathing frequency (fR) is no longer under chemoreflex control during REM sleep

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dc.contributor.author Burke, Peter
dc.contributor.author Kanbar, Roy
dc.contributor.author Basrting, Tyler
dc.contributor.author Viar, Kenneth
dc.contributor.author Stornetta, Ruth
dc.contributor.author Guyenet, Patrice
dc.date.accessioned 2016-10-11T10:21:19Z
dc.date.available 2016-10-11T10:21:19Z
dc.date.copyright 2015 en_US
dc.date.issued 2016-10-11
dc.identifier.issn 0892-6638 en_US
dc.identifier.uri http://hdl.handle.net/10725/4565
dc.description.abstract Objective: To define the contribution of central chemoreception in general and the retrotrapezoid nucleus (RTN) in particular to the regulation of breathing in REM sleep. Methods: EEG, neck EMG, blood pressure, fR and tidal volume (VT) were recorded in 23 conscious adult male Sprague-Dawley rats. RTN was optogenetically stimulated with channelrhodopsin-2 (ChR2, 20s) or inhibited with archaerhodopsin (Arch; 10 s) during natural sleep and quiet wake periods. ChR2 and Arch were delivered using previously described PRSX8-promoter containing lentiviral vectors. Main Results: In quiet wake or non-REM sleep, hypercapnia (3 or 6% FiCO2) increased both fR and VT; in REM sleep, hypercapnia increased VT but fR was unaffected. Optogenetic inhibition of RTN neurons reduced VT in all three states but reduced fR only during quiet wake and non-REM sleep. Optogenetic stimulation of RTN neurons always increased VT but raised fR only in quiet wake and non-REM sleep. Phasic stimulation of RTN at frequencies above resting fR entrained and shortened the breathing cycle except in REM sleep. Phasic RTN stimulation produced active expiration only during wake and increased fR exclusively by reducing the duration of the post-inspiratory phase. Conclusions: During REM sleep, VT regulation by both hypercarbia and RTN is retained but the overall hypercapnic ventilatory reflex is reduced because fR is no longer under chemoreceptor control. Furthermore, respiratory drive contributed by RTN is remarkably state-dependent, active expiration being elicited only during wake and tachypnea only during non-REM sleep and quiet wake. en_US
dc.language.iso en en_US
dc.title Breathing frequency (fR) is no longer under chemoreflex control during REM sleep en_US
dc.type Article en_US
dc.description.version Published en_US
dc.author.school SOP en_US
dc.author.idnumber 201005298 en_US
dc.author.department N/A en_US
dc.description.embargo N/A en_US
dc.relation.journal The FASEB Journal en_US
dc.journal.volume 29 en_US
dc.journal.issue 1_Suppl. en_US
dc.identifier.ctation Burke, P., Kanbar, R., Basting, T., Viar, K., Stornetta, R., & Guyenet, P. (2015). Breathing frequency (fR) is no longer under chemoreflex control during REM sleep. The FASEB Journal, 29(1_supplement), 1012-16. en_US
dc.author.email roy.kanbar@lau.edu.lb en_US
dc.identifier.tou http://libraries.lau.edu.lb/research/laur/terms-of-use/articles.php en_US
dc.identifier.url http://www.fasebj.org/content/29/1_Supplement/1012.16.short en_US
dc.orcid.id https://orcid.org/0000-0001-5450-6443 en_US

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