{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T16:12:54Z","timestamp":1761581574607,"version":"3.37.3"},"reference-count":58,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2017,7,3]],"date-time":"2017-07-03T00:00:00Z","timestamp":1499040000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000071","name":"National Institute of Child Health and Human Development","doi-asserted-by":"publisher","award":["36379"],"award-info":[{"award-number":["36379"]}],"id":[{"id":"10.13039\/100000071","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2017,8]]},"abstract":"<jats:sec><jats:title>New Findings<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p><jats:bold>What is the central question of this study?<\/jats:bold><\/jats:p>\n<jats:p>Does activation of serotonergic neurons in the caudal medullary raphe, some of which project to the nucleus of the solitary tract, shorten the laryngeal chemoreflex?<\/jats:p>\n<\/jats:list-item>\n<jats:list-item><jats:p><jats:bold>What is the main finding and its importance?<\/jats:bold><\/jats:p>\n<jats:p>We found that serotonin originating from neurons in the caudal raphe acts through a 5\u2010HT<jats:sub>3<\/jats:sub> receptor located in the nucleus of the solitary tract to terminate reflex apnoea. Failure or deficiency of this arousal\u2010related process is likely to be relevant to the pathogenesis of sudden infant death syndrome.<\/jats:p>\n<\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec><jats:sec><jats:label\/><jats:p>Failure to terminate apnoea and arouse is likely to contribute to sudden infant death syndrome (SIDS). Serotonin is deficient in the brainstems of babies who have died of SIDS. We tested the hypothesis that activation of serotoninergic neurons in the caudal medullary raphe, some of which project to the nucleus of the solitary tract (NTS), would shorten the laryngeal chemoreflex (LCR). We studied anaesthetized neonatal rat pups between postnatal days 9 and 17. We injected 5\u201340\u00a0\u03bcl of water into the larynx to elicit the LCR and measured the duration of respiratory disruption. Microinjection of 50\u00a0nl of 100\u00a0\u03bc<jats:sc>m<\/jats:sc> AMPA into the caudal medullary raphe shortened the apnoeas (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.001) and respiratory inhibition (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.005) associated with the LCR. When 50\u00a0nl of 30\u00a0m<jats:sc>m<\/jats:sc> ondansetron, a 5\u2010HT<jats:sub>3<\/jats:sub> antagonist, was microinjected bilaterally into the NTS, AMPA microinjected into the caudal raphe no longer shortened the LCR. After bilateral microinjection of vehicle into the NTS, AMPA microinjection into the caudal raphe significantly shortened the LCR. AMPA, a glutamate receptor agonist, may activate many neurons within the caudal raphe, but blocking the 5\u2010HT<jats:sub>3<\/jats:sub> receptor\u2010dependent responses in the NTS prevented the shortening of the LCR associated with AMPA microinjections into the caudal raphe. Thus, serotonin originating from neurons in the caudal raphe acts through a 5\u2010HT<jats:sub>3<\/jats:sub> receptor located in the NTS to terminate or shorten the LCR. Serotonin is deficient in the brainstems of babies who have died of SIDS, and deficient serotonergic termination of apnoea is likely to be relevant to the pathogenesis of SIDS.<\/jats:p><\/jats:sec>","DOI":"10.1113\/ep086082","type":"journal-article","created":{"date-parts":[[2017,7,4]],"date-time":"2017-07-04T13:22:02Z","timestamp":1499174522000},"page":"1007-1018","source":"Crossref","is-referenced-by-count":9,"title":["Activation of serotonergic neurons in the medullary caudal raphe shortens the laryngeal chemoreflex in anaesthetized neonatal rats"],"prefix":"10.1113","volume":"102","author":[{"given":"William T.","family":"Donnelly","sequence":"first","affiliation":[{"name":"Department of Molecular and Systems Biology Geisel School of Medicine at Dartmouth  Lebanon NH USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Luxi","family":"Xia","sequence":"additional","affiliation":[{"name":"Department of Molecular and Systems Biology Geisel School of Medicine at Dartmouth  Lebanon NH USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Donald","family":"Bartlett","sequence":"additional","affiliation":[{"name":"Department of Molecular and Systems Biology Geisel School of Medicine at Dartmouth  Lebanon NH USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8572-6035","authenticated-orcid":false,"given":"J. 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