{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T18:40:00Z","timestamp":1791398400757,"version":"4.3.3"},"reference-count":50,"publisher":"National Academy of Sciences","issue":"37","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2010,9,14]]},"abstract":"<jats:p>\n                    There is a long-standing controversy about the role of serotonin in sleep\/wake control, with competing theories that it either promotes sleep or causes arousal. Here, we show that there is a marked increase in wakefulness when all serotonin neurons are genetically deleted in mice hemizygous for ePet1-Cre and homozygous for floxed\n                    <jats:italic>Lmx1b<\/jats:italic>\n                    (\n                    <jats:italic>\n                      Lmx1b\n                      <jats:sup>f\/f\/p<\/jats:sup>\n                    <\/jats:italic>\n                    ). However, this only occurs at cool ambient temperatures and can be explained by a thermoregulatory defect that leads to an increase in motor activity to generate heat. Because some serotonin neurons are stimulated by CO\n                    <jats:sub>2<\/jats:sub>\n                    , and serotonin activates thalamocortical networks, we hypothesized that serotonin neurons cause arousal in response to hypercapnia. We found that\n                    <jats:italic>\n                      Lmx1b\n                      <jats:sup>f\/f\/p<\/jats:sup>\n                    <\/jats:italic>\n                    mice completely lacked any arousal response to inhalation of 10% CO\n                    <jats:sub>2<\/jats:sub>\n                    (with 21% O\n                    <jats:sub>2<\/jats:sub>\n                    in balance N\n                    <jats:sub>2<\/jats:sub>\n                    ) but had normal arousal responses to hypoxia, sound, and air puff. We propose that serotonin neurons mediate the potentially life-saving arousal response to hypercapnia. Impairment of this response may contribute to sudden unexpected death in epilepsy, sudden infant death syndrome, and sleep apnea.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1004587107","type":"journal-article","created":{"date-parts":[[2010,8,30]],"date-time":"2010-08-30T22:49:18Z","timestamp":1283208558000},"page":"16354-16359","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":231,"title":["Central serotonin neurons are required for arousal to CO\n                    <sub>2<\/sub>"],"prefix":"10.1073","volume":"107","author":[{"given":"Gordon F.","family":"Buchanan","sequence":"first","affiliation":[{"name":"Departments of aNeurology and"},{"name":"Veterans Affairs Medical Center, West Haven, CT 06516"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"George B.","family":"Richerson","sequence":"additional","affiliation":[{"name":"Departments of aNeurology and"},{"name":"Cellular and Molecular Physiology, Yale University, New Haven, CT 06520; and"},{"name":"Veterans Affairs Medical Center, West Haven, CT 06516"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2010,8,30]]},"reference":[{"key":"e_1_3_3_1_2","first-page":"24S","article-title":"Sleep and serotonin: An unfinished story","volume":"21","author":"Jouvet M","year":"1999","unstructured":"M Jouvet, Sleep and serotonin: An unfinished story. 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