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HIGHLIGHTED TOPICS
Oxygen Sensing in Health and Disease

Intermittent hypoxia induces transient arousal delay in newborn mice

¹Laboratoire de Neurologie et Physiologie du Développement, INSERM E9935, Hôpital Robert-Debré, 75019 Paris; ²Service de Physiologie-Explorations Fonctionnelles, Hôpital Raymond-Poincaré, 92380 Garches; ³Service de Pédiatrie-Réanimation, Hôpital Robert-Debré, 75019 Paris; ⁴URAPC, Université de Picardie, 80036 Amiens; and ⁵Service de Physiologie, Hôpital Robert-Debré, 75019 Paris, France

Submitted 30 July 2003 ; accepted in final form 22 October 2003

Previous studies suggested that defective arousal might be a major mechanism in sleep-disordered breathing such as sudden infant death syndrome and obstructive sleep apnea. In this study, we examined the effects of intermittent hypoxia (IH) on the arousal response to hypoxia in 4-day-old mice. We hypothesized that IH would increase arousal latency, as previously reported in other species, and we measured the concomitant changes in ventilation to shed light on the relationship between breathing and arousal. Arousal was scored according to behavioral criteria. Breathing variables were measured noninvasively by use of whole-body flow plethysmography. In the hypoxic group (n = 14), the pups were exposed to 5% O₂ in N₂ for 3 min and returned to air for 6 min. This test was repeated eight times. The normoxic mice (n = 14) were constantly exposed to normoxia. The hypoxic mice showed a 60% increase in arousal latency (P < 0.0001). Normoxic controls showed virtually no arousals. IH depressed normoxic ventilation below baseline prehypoxic levels, while preserving the ventilatory response to hypoxia. The breathing pattern and arousal responses recovered fully after 2 h of normoxia. We conclude that IH rapidly and reversibly depressed breathing and delayed arousal in newborn mice. Both effects may be due to hypoxia-induced release of inhibitory neurotransmitters acting concomitantly on both functions.

control of breathing; sleep; development

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