4.3 Article

Cold stimulates the behavioral response to hypoxia in newborn mice

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.90582.2008

Keywords

arousal; chemosensitivity; control of breathing

Categories

Funding

  1. INSERM
  2. Chancellerie des Universites
  3. Garches Foundation
  4. Marguerite-Marie Delacroix Foundation
  5. Research Foundation Flanders (FWO)

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Bollen B, Bouslama M, Matrot B, Rotrou Y, Vardon G, Lofaso F, Van den Bergh O, D'Hooge R, Gallego J. Cold stimulates the behavioral response to hypoxia in newborn mice. Am J Physiol Regul Integr Comp Physiol 296: R1503-R1511, 2009. First published March 18, 2009; doi: 10.1152/ajpregu.90582.2008.- In newborns, hypoxia elicits increased ventilation, arousal followed by defensive movements, and cries. Cold is known to affect the ventilatory response to hypoxia, but whether it affects the arousal response remains unknown. The aim of the present study was to assess the effects of cold on the ventilatory and arousal responses to hypoxia in newborn mice. We designed an original platform measuring noninvasively and simultaneously the breathing pattern by whole body plethysmography, body temperature by infrared thermography, as well as motor and ultrasonic vocal (USV) responses. Six-day-old mice were exposed twice to 10% O-2 for 3 min at either cold temperature (26 degrees C) or thermoneutrality (33 degrees C). At 33 degrees C, hypoxia elicited a marked increase in ventilation followed by a small ventilatory decline, small motor response, and almost no USVs. Body temperature was not influenced by hypoxia, and oxygen consumption (<(V)over dot>O-2) displayed minimal changes. At 26 degrees C, hypoxia elicited a slight increase in ventilation with a large ventilatory decline and a large drop of <(V)over dot>O-2. This response was accompanied by marked USV and motor responses. Hypoxia elicited a small decrease in temperature after the return to normoxia, thus precluding any causal influence on the motor and USV responses to hypoxia. In conclusion, cold stimulated arousal and stress responses to hypoxia, while depressing hypoxic hyperpnea. Arousal is an important defense mechanism against sleep-disordered breathing. The dissociation between ventilatory and behavioral responses to hypoxia suggests that deficits in the arousal response associated with sleep breathing disorders cannot be attributed to a depressed hypoxic response.

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