文章基本信息

标题：Central serotonin neurons are required for arousal to CO2
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作者：Gordon F. Buchanan ; George B. Richerson
期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2010
卷号：107
期号：37
页码：16354-16359
DOI：10.1073/pnas.1004587107
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：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 Lmx1b (Lmx1bf/f/p). 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 CO2, and serotonin activates thalamocortical networks, we hypothesized that serotonin neurons cause arousal in response to hypercapnia. We found that Lmx1bf/f/p mice completely lacked any arousal response to inhalation of 10% CO2 (with 21% O2 in balance N2) 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.
关键词：chemoreception ; hypercapnia ; sleep ; thermoregulation ; Lmx1b