AbstractAim:  To study the ventilatory and arousal/defence responses to hypoxia in newborn mutant mice lacking the β2 subunit of the nicotinic acetylcholine receptors.Methods:  Breathing variables were measured non‐invasively in mutant (n =31) and wild‐type age‐matched mice (n = 57) at 2 and 8 days of age using flow barometric whole‐body plethysmography. The arousal/defence response to hypoxia was determined using behavioural criteria.Results:  On day 2, mutant pups had significantly greater baseline ventilation (16%) than wild‐type pups (P < 0.02). Mutant pups had a decreased hypoxic ventilatory declines. Arousal latency was significantly shorter in mutant than in wild‐type pups (133 ± 40 vs. 146 ± 20 s, respectively, P < 0.026). However, the duration of movement elicited by hypoxia was shorter in mutant than in wild‐type pups (14.7 ± 5.9 vs. 23.0 ± 10.7 s, respectively, P < 0.0005). Most differences disappeared on P8, suggesting a high degree of functional plasticity.Conclusion:  The blunted hypoxic ventilatory decline and the shorter arousal latency on day 2 suggested that disruption of the β2 nicotinic acetylcholine receptors impaired inhibitory processes affecting both the ventilatory and the arousal response to hypoxia during postnatal development.