{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T17:09:45Z","timestamp":1791306585681,"version":"4.3.1"},"reference-count":49,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2011,9]]},"abstract":"<jats:p> Mice deficient in the transcription factor Pet-1<jats:sup>\u2212\/\u2212<\/jats:sup> have a \u223c70% deficiency of brainstem serotonin [5-hydroxytryptamine (5-HT)] neurons and exhibit spontaneous bradycardias in room air at postnatal day (P)5 and P12 and delayed gasping in response to a single episode of anoxia at P4.5 and P9.5 (Cummings KJ, Li A, Deneris ES, Nattie EE. Am J Physiol Regul Integr Comp Physiol 298: R1333\u2013R1342, 2010; and Erickson JT, Sposato BC. J Appl Physiol 106: 1785\u20131792, 2009). We hypothesized that at a critical age Pet-1<jats:sup>\u2212\/\u2212<\/jats:sup> mice will fail to autoresuscitate during episodic anoxia, ultimately dying from a failure of gasping to restore heart rate (HR). We exposed P5, P8, and P12 Pet-1<jats:sup>\u2212\/\u2212<\/jats:sup> mice and wild-type littermates (WT) to four 30-s episodes of anoxia (97% N<jats:sub>2<\/jats:sub>-3% CO<jats:sub>2<\/jats:sub>), separated by 5 min of room air. We observed excess mortality in Pet-1<jats:sup>\u2212\/\u2212<\/jats:sup> only at P8: 43% of Pet-1<jats:sup>\u2212\/\u2212<\/jats:sup> animals survived past the third episode of anoxia while \u223c95% of WT survived all four episodes ( P = 0.004). No deaths occurred at P5 and at P12, and one of six Pet-1<jats:sup>\u2212\/\u2212<\/jats:sup> mice died after the fourth episode, while all WT animals survived. At P8, dying Pet-1<jats:sup>\u2212\/\u2212<\/jats:sup> animals had delayed gasping, recovery of HR, and eupnea after the first two episodes of anoxia ( P &lt; 0.001 for each); death ultimately occurred when gasping failed to restore HR. Both high- and low-frequency components of HR variability were abnormally elevated in dying Pet-1<jats:sup>\u2212\/\u2212<\/jats:sup> animals following the first episode of anoxia. Dying P8 Pet-1<jats:sup>\u2212\/\u2212<\/jats:sup> animals had significantly fewer 5-HT neurons in the raphe magnus than surviving animals ( P &lt; 0.001). Our data indicate a critical developmental window at which a brainstem 5-HT deficiency increases the risk of death during episodes of anoxia. They may apply to the sudden infant death syndrome, which occurs at a critical age and is associated with 5-HT deficiency. <\/jats:p>","DOI":"10.1152\/japplphysiol.00336.2011","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T23:22:12Z","timestamp":1308352932000},"page":"825-833","source":"Crossref","is-referenced-by-count":68,"title":["Failed heart rate recovery at a critical age in 5-HT-deficient mice exposed to episodic anoxia: implications for SIDS"],"prefix":"10.1152","volume":"111","author":[{"given":"Kevin J.","family":"Cummings","sequence":"first","affiliation":[{"name":"Department of Physiology and Neurobiology, Dartmouth Medical School, Lebanon, New Hampshire; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kathryn G.","family":"Commons","sequence":"additional","affiliation":[{"name":"Departments of 2Anesthesiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie 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