Proton detection and breathing regulation by the retrotrapezoid nucleus

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dc.contributor.author Guyenet, Patrice G.
dc.contributor.author Bayliss, Douglas A.
dc.contributor.author Stornetta, Ruth L.
dc.contributor.author Ludwig, Marie-Gabrielle
dc.contributor.author Kumar, Natasha N.
dc.contributor.author Shi, Yingtang
dc.contributor.author Burke, Peter G. R.
dc.contributor.author Kanbar, Roy
dc.contributor.author Basting, Tyler M.
dc.contributor.author Holloway, Benjamin B.
dc.contributor.author Wenker, Ian C.
dc.date.accessioned 2016-10-11T08:55:40Z
dc.date.available 2016-10-11T08:55:40Z
dc.date.copyright 2016 en_US
dc.date.issued 2016-10-11
dc.identifier.issn 0022-3751 en_US
dc.identifier.uri http://hdl.handle.net/10725/4561
dc.description.abstract Abstract We discuss recent evidence which suggests that the principal central respiratory chemoreceptors are located within the retrotrapezoid nucleus (RTN) and that RTN neurons are directly sensitive to [H+]. RTN neurons are glutamatergic. In vitro, their activation by [H+] requires expression of a proton-activated G protein-coupled receptor (GPR4) and a proton-modulated potassium channel (TASK-2) whose transcripts are undetectable in astrocytes and the rest of the lower brainstem respiratory network. The pH response of RTN neurons is modulated by surrounding astrocytes but genetic deletion of RTN neurons or deletion of both GPR4 and TASK-2 virtually eliminates the central respiratory chemoreflex. Thus, although this reflex is regulated by innumerable brain pathways, it seems to operate predominantly by modulating the discharge rate of RTN neurons, and the activation of RTN neurons by hypercapnia may ultimately derive from their intrinsic pH sensitivity. RTN neurons increase lung ventilation by stimulating multiple aspects of breathing simultaneously. They stimulate breathing about equally during quiet wake and non-rapid eye movement (REM) sleep, and to a lesser degree during REM sleep. The activity of RTN neurons is regulated by inhibitory feedback and by excitatory inputs, notably from the carotid bodies. The latter input operates during normo- or hypercapnia but fails to activate RTN neurons under hypocapnic conditions. RTN inhibition probably limits the degree of hyperventilation produced by hypocapnic hypoxia. RTN neurons are also activated by inputs from serotonergic neurons and hypothalamic neurons. The absence of RTN neurons probably underlies the sleep apnoea and lack of chemoreflex that characterize congenital central hypoventilation syndrome. en_US
dc.language.iso en en_US
dc.title Proton detection and breathing regulation by the retrotrapezoid nucleus 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 Journal of Physiology en_US
dc.journal.volume 594 en_US
dc.journal.issue 6 en_US
dc.article.pages 1529-1551 en_US
dc.identifier.doi https://doi.org/10.1113/JP271480 en_US
dc.identifier.ctation Guyenet, P. G., Bayliss, D. A., Stornetta, R. L., Ludwig, M. G., Kumar, N. N., Shi, Y., ... & Wenker, I. C. (2016). Proton detection and breathing regulation by the retrotrapezoid nucleus. The Journal of physiology 594 (6), 1529-1551 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 https://physoc.onlinelibrary.wiley.com/doi/full/10.1113/JP271480 en_US
dc.orcid.id https://orcid.org/0000-0001-5450-6443 en_US

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