Abstract

Onset and ontogeny of the O 2 chemoreceptive control of ventilation was investigated in Xenopus laevis. The density and size of branchial serotonin-immunoreactive neuroepithelial cells (5-HT-IR NECs) were also determined using confocal immunofluorescent microscopy. Larvae started gill ventilation at 3 days post-fertilization (dpf), and, at this early stage, acute hypoxic exposure produced an increase in frequency from 28 ± 4 to 60 ± 2 beats .min − 1 . Concurrent with the onset of ventilatory responses, 5-HT-IR NECs appeared in the gill filament bud. Lung ventilation began at 5 dpf and exhibited a 3-fold increase in frequency during acute hypoxia. At 10 dpf, gill ventilatory sensitivity to hypoxia increased, as did NEC density, from 15 ± 1 (5 dpf) to 29 ± 2 (10 dpf) cells .mm of filament −1. Unlike ventilation frequency, gill ventilation amplitude and lung expired volume were unaltered by acute hypoxia. Chronic exposure to moderate hypoxia, at a P o 2 of 110 mmHg, attenuated acute responses to moderate hypoxia at 10 and 14 dpf but had no effect at more severe hypoxia or at other stages. Chronic hypoxia also stimulated 5-HT-IR NECs growth at 21 dpf. Collectively, larvae at 5 dpf exhibited strong O 2-driven gill and lung ventilatory responses, and between 10 and 21 dpf, the early hypoxic responses can be shaped by the ambient P o 2.

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