Interdependent feedback regulation of breathing by the carotid bodies and 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 Kanbar, Roy
dc.contributor.author Shi, Yingtang
dc.date.accessioned 2017-12-15T11:37:20Z
dc.date.available 2017-12-15T11:37:20Z
dc.date.copyright 2017 en_US
dc.date.issued 2017-12-15
dc.identifier.issn 0022-3751 en_US
dc.identifier.uri http://hdl.handle.net/10725/6799
dc.description.abstract The retrotrapezoid nucleus, RTN, regulates breathing in a CO2 and state-dependent manner. RTN neurons are glutamatergic and innervate principally the respiratory pattern generator; they regulate multiple aspects of breathing, including active expiration, and maintain breathing automaticity during non-REM sleep. RTN neurons encode arterial PCO2 /pH via cell-autonomous and paracrine mechanisms, and via input from other CO2-responsive neurons. In short, RTN neurons are a pivotal structure for breathing automaticity and arterial PCO2 homeostasis. The carotid bodies stimulate the respiratory pattern generator directly and, indirectly, by activating RTN via a neuronal projection originating within the solitary tract nucleus. The indirect pathway operates under normo- or hypercapnic conditions; under respiratory alkalosis (e.g. hypoxia) RTN neurons are silent and the excitatory input from the carotid bodies is suppressed. Also, silencing RTN neurons optogenetically quickly triggers a compensatory increase in carotid body activity. Thus, in conscious mammals, breathing is subject to a dual and interdependent feedback regulation by chemoreceptors. Depending on the circumstance, the activity of the carotid bodies and that of RTN vary in the same or the opposite direction, producing additive or countervailing effects on breathing. These interactions are mediated either via changes in blood gases or by brainstem neuronal connections but their ultimate effect is invariably to minimize arterial PCO2 fluctuations. We discuss the potential relevance of this dual chemoreceptor feedback to cardiorespiratory abnormalities present in diseases in which the carotid bodies are hyperactive at rest, e.g. essential hypertension, obstructive sleep apnea and heart failure. en_US
dc.language.iso en en_US
dc.title Interdependent feedback regulation of breathing by the carotid bodies and 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 Pharmaceutical Sciences Department en_US
dc.description.embargo N/A en_US
dc.relation.journal Journal of Physiology en_US
dc.journal.volume 596
dc.journal.issue 15 en_US
dc.article.pages 3029-3042 en_US
dc.identifier.doi https://doi.org/10.1113/JP274357 en_US
dc.identifier.ctation Guyenet, P. G., Bayliss, D. A., Stornetta, R. L., Kanbar, R., Shi, Y., Holloway, B. B., ... & Wenker, I. C. (2018). Interdependent feedback regulation of breathing by the carotid bodies and the retrotrapezoid nucleus. The Journal of physiology, 596(15), 3029-3042. 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/JP274357 en_US
dc.orcid.id https://orcid.org/0000-0001-5450-6443
dc.author.affiliation Lebanese American University en_US

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