{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T17:09:51Z","timestamp":1791306591864,"version":"4.3.1"},"reference-count":76,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2016,6,12]],"date-time":"2016-06-12T00:00:00Z","timestamp":1465689600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2016,7]]},"abstract":"<jats:title>New Findings<\/jats:title><jats:sec><jats:label\/><jats:p><jats:list list-type=\"bullet\"><jats:list-item><jats:p><jats:bold>What is the central question of this study?<\/jats:bold><\/jats:p><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 died of SIDS. Therefore, we tested the hypothesis that serotonin in the nucleus of the solitary tract (NTS) would shorten reflex apnoea.<\/jats:p><\/jats:list-item><jats:list-item><jats:p><jats:bold>What is the main finding and its importance?<\/jats:bold><\/jats:p><jats:p>Serotonin microinjected into the NTS shortened the apnoea and respiratory inhibition associated with the laryngeal chemoreflex. Moreover, this effect was achieved through a 5\u2010HT<jats:sub>3<\/jats:sub>receptor. This is a new insight that is likely to be relevant to the pathogenesis of SIDS.<\/jats:p><\/jats:list-item><\/jats:list><\/jats:p><\/jats:sec><jats:sec><jats:label\/><jats:p>The laryngeal chemoreflex (LCR), an airway\u2010protective reflex that causes apnoea and bradycardia, has long been suspected as an initiating event in the sudden infant death syndrome. Serotonin (5\u2010HT) and 5\u2010HT receptors may be deficient in the brainstems of babies who die of sudden infant death syndrome, and 5\u2010HT seems to be important in terminating apnoeas directly or in causing arousals or as part of the process of autoresuscitation. We hypothesized that 5\u2010HT in the brainstem would limit the duration of the LCR. We studied anaesthetized rat pups between 7 and 21 days of age and made microinjections into the cisterna magna or into the nucleus of the solitary tract (NTS). Focal, bilateral microinjections of 5\u2010HT into the caudal NTS significantly shortened the LCR. The 5\u2010HT<jats:sub>1a<\/jats:sub>receptor antagonist, WAY 100635, did not affect the LCR consistently, nor did a 5\u2010HT<jats:sub>2<\/jats:sub>receptor antagonist, ketanserin, alter the duration of the LCR. The 5\u2010HT<jats:sub>3<\/jats:sub>specific agonist, 1\u2010(3\u2010chlorophenyl)\u2010biguanide, microinjected bilaterally into the caudal NTS significantly shortened the LCR. Thus, endogenous 5\u2010HT released within the NTS may curtail the respiratory depression that is part of the LCR, and serotonergic shortening of the LCR may be attributed to activation of 5\u2010HT<jats:sub>3<\/jats:sub>receptors within the NTS. 5\u2010HT<jats:sub>3<\/jats:sub>receptors are expressed presynaptically on C\u00a0fibre afferents of the superior laryngeal nerve, and serotonergic shortening of the LCR may be mediated presynaptically by enhanced activation of inhibitory interneurons within the NTS.<\/jats:p><\/jats:sec>","DOI":"10.1113\/ep085716","type":"journal-article","created":{"date-parts":[[2016,4,28]],"date-time":"2016-04-28T00:38:31Z","timestamp":1461803911000},"page":"946-961","source":"Crossref","is-referenced-by-count":23,"title":["Serotonin in the solitary tract nucleus shortens the laryngeal chemoreflex in anaesthetized neonatal rats"],"prefix":"10.1113","volume":"101","author":[{"given":"William T.","family":"Donnelly","sequence":"first","affiliation":[{"name":"Department of Physiology and Neurobiology Geisel School of Medicine at Dartmouth Lebanon NH 03756 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr","given":"Donald","family":"Bartlett","sequence":"additional","affiliation":[{"name":"Department of Physiology and Neurobiology Geisel School of Medicine at Dartmouth Lebanon NH 03756 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8572-6035","authenticated-orcid":false,"given":"J. 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