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This Article Full Text Full Text (PDF) All Versions of this Article: 540/2/691    most recent 2001.014464v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Cohen, G. Articles by Gaultier, C. Search for Related Content PubMed PubMed Citation Articles by Cohen, G. Articles by Gaultier, C.

Depression of hypoxic arousal response in adolescent mice following antenatal vasoactive intestinal polypeptide blockade

Gary Cohen, Pierre Gressens, Jorge Gallego and Claude Gaultier

Late-gestation blockade of vasoactive intestinal polypeptide (VIP) activity in pregnant mice produces discrete morphological abnormalities in the somatosensory cortex of offspring. We investigated the functional implications of this lesion on the behavioural arousal response to moderate hypoxia. Pregnant mice received twice-daily injections of 200 µl saline (control), or saline + 50 µg VIP antagonist (anti-VIP) on embryonic days 17 and 18. Offspring were studied unrestrained at 6-7 weeks after birth, in a bias-flow whole-body plethysmograph during behavioural quiet sleep. Arousal was defined by movement (MVT) lasting ≥1 s. Hypoxic ventilatory (HVR) and arousal responses were measured during a 5 min exposure to 10 % O₂-3 % CO₂ (hypoxia); peripheral chemoreflex drive was estimated by transient hyperoxia administered at rest and end-hypoxia (Dejours-type test). MVTs increased in all mice during hypoxia, but in anti-VIP mice: (a) MVT onset was delayed (174 ± 90 vs. 108 ± 59 s from the start of hypoxia, anti-VIP vs. control; P = 0.008); and (b) MVTs were less frequent, and total MVT time in hypoxia was less (8 ± 7 vs. 15 ± 9 %; P = 0.03). The HVR, and peripheral drive at rest and end-hypoxia were comparable in control and anti-VIP mice. In conclusion, a significant arousal deficit was evident in anti-VIP mice. This was not associated with obviously deranged peripheral or brainstem-mediated responses to hypoxia during sleep. This may signal a general deficit in the way hypoxic distress is monitored and processed, and arousal initiated and sustained in these mice.

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