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Control of breathing in newborn mice lacking the beta-2 nAChR subunit.

Abstract : AIM: To study the ventilatory and arousal/defence responses to hypoxia in newborn mutant mice lacking the beta2 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 beta2 nicotinic acetylcholine receptors impaired inhibitory processes affecting both the ventilatory and the arousal response to hypoxia during postnatal development.
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Submitted on : Tuesday, July 17, 2007 - 3:51:21 PM
Last modification on : Wednesday, September 23, 2020 - 4:34:14 AM

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S. Dauger, E. Durand, G. Cohen, H. Lagercrantz, J.-P. Changeux, et al.. Control of breathing in newborn mice lacking the beta-2 nAChR subunit.. Acta Physiologica Scandinavica, Wiley-Blackwell, 2004, 182 (2), pp.205-12. ⟨10.1111/j.1365-201X.2004.01345.x⟩. ⟨pasteur-00163485⟩

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