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Hypoxia, but not Hypercapnia Evokes the Arousal Response During Sleep in Mice
Author(s) -
Ramirez Sanja,
Rubens Daniel,
Pillai Aiswarya Pillai,
Allen Travis,
Ramirez Jan
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.1012.17
Subject(s) - hypercapnia , arousal , hypoxia (environmental) , stimulus (psychology) , hypoxic ventilatory response , psychology , medicine , anesthesia , respiratory system , neuroscience , chemistry , oxygen , organic chemistry , psychotherapist
One of the most established risk factor for SIDS is an infant sleeping in prone position. This position exposes the child to hypoxia and hypercapnia, which should normally lead to an arousal response that wakes up the child. It is thought that the failure to arouse is an important first step in the events leading to the death of the child. Here we explored the differential roles of hypoxia and hypercapnia in the generation of the arousal response during natural sleep using CD‐1 mice as an animal model. Mice were observed in a full‐body plethysmograph during natural sleep while exposing the animals to hypoxic (100% N 2 ) and hypercapnic stimuli (gas composition of 21% O 2 5% CO 2 balanced N 2 ). We demonstrate that the hypoxic stimuli evoked a whole body arousal response in all mice within less than 15 seconds. The hypercapnic stimulus reliably evoked a respiratory response consisting of an increase in breathing frequency and tidal volume. However, mice lacked a whole body arousal response and did not wake up even if the hypercapnic stimulus was continued for 5 minutes. We conclude that in these mice the arousal response is triggered by hypoxia and not hypercapnia. Moreover, our study suggests that the presence of a hypercapnic ventilatory response is not automatically indicative for arousal. Ongoing studies explore the interaction between the hypercapnic and hypoxic response and the failed arousal seen in mice with inner ear defect. Our study has important implications in understanding the mechanisms that lead to failed arousal in SIDS.