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Arousal in rat pups habituates in response to repeated bouts of hypercapnia: implications for the Sudden Infant Death Syndrome (SIDS)
Author(s) -
Darnall Robert A,
Schneider Robert,
Webster Caroline,
Tobia Chritine
Publication year - 2012
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.26.1_supplement.704.16
Subject(s) - hypercapnia , arousal , hypoxia (environmental) , sudden infant death syndrome , anesthesia , habituation , medicine , chemoreceptor , psychology , chemistry , neuroscience , audiology , oxygen , acidosis , pediatrics , receptor , organic chemistry
In infants, arousal from sleep is an important protective response against hypoxia and hypercapnia. In rat pups, arousal in response to hypoxia habituates with a progressive lengthening of the time to arousal (latency) over repeated bouts. We hypothesized that arousal habituation (AH) would also occur with repeated bouts of hypercapnia and would involve carotid chemoreceptors. We exposed 177 rat pups (P9–P20) to 4 or 8 three minute exposures to either 8% CO2 in room air (CO2/RA), 8% CO2 in 100% O2 (CO2/100%O2), 8% CO2 + 10% O2 (CO2/10%O2), 100% O2 (100%O2), or room air (RA), alternating with 6 minutes of RA. Exposures were begun during sleep and arousal was assessed using behavioral criteria. Arousal latency progressively increased with each exposure to all CO2 containing gas mixtures and mean latencies were shorter than when exposed to either RA or 100%O2 controls. Mean arousal latency was shortest in CO2/10%O2. Arousal latencies with CO2/O2 were longer than those with CO2/RA during trials 5–8. Our results indicate that AH occurs in response to repeated bouts of hypercapnia. The combination of hypercapnia and hypoxia is a more potent arousal stimulus than CO2 alone. Exposure to CO2/O2 resulted in more AH than CO2/RA, suggesting carotid chemoreceptor involvement. AH may prevent adequate protective responses to subsequent exposures to hypoxia and hypercapnia increasing the risk for SIDS. NIHPO1HD36379