期刊
ELIFE
卷 5, 期 -, 页码 -出版社
eLIFE SCIENCES PUBL LTD
DOI: 10.7554/elife.14170
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类别
资金
- Karolinska Institutet
- Vetenskapsradet [2010-4392, 2013-3189, 2008-5829, 2009-3724]
- Hjarnfonden [FO2014+0220, FO2011-008, FO2012-0036, FO2015-0020]
- VINNOVA Future Health Innovation grant [2010-00534]
- Stockholms Lans Landsting [2011-0095, 2012-0465, 2014-0011]
- Swedish National Heart and Lung foundation [20120373, 20150558]
- Knut och Alice Wallenbergs Stiftelse [102179]
- Freemasons' Children's House
- Axel Tielman Foundation [2015-00220]
- Fraenckel Foundation [FRAE0018]
Inflammation-induced release of prostaglandin E-2 (PGE(2)) changes breathing patterns and the response to CO2 levels. This may have fatal consequences in newborn babies and result in sudden infant death. To elucidate the underlying mechanisms, we present a novel breathing brainstem organotypic culture that generates rhythmic neural network and motor activity for 3 weeks. We show that increased CO2 elicits a gap junction-dependent release of PGE(2). This alters neural network activity in the preBotzinger rhythm-generating complex and in the chemosensitive brainstem respiratory regions, thereby increasing sigh frequency and the depth of inspiration. We used mice lacking eicosanoid prostanoid 3 receptors (EP3R), breathing brainstem organotypic slices and optogenetic inhibition of EP3R(+/+) cells to demonstrate that the EP3R is important for the ventilatory response to hypercapnia. Our study identifies a novel pathway linking the inflammatory and respiratory systems, with implications for inspiration and sighs throughout life, and the ability to autoresuscitate when breathing fails.
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