| First Author | Dauger S | Year | 2004 |
| Journal | Acta Physiol Scand | Volume | 182 |
| Issue | 2 | Pages | 205-12 |
| PubMed ID | 15450117 | Mgi Jnum | J:102005 |
| Mgi Id | MGI:3606387 | Doi | 10.1111/j.1365-201X.2004.01345.x |
| Citation | Dauger S, et al. (2004) Control of breathing in newborn mice lacking the beta-2 nAChR subunit. Acta Physiol Scand 182(2):205-12 |
| abstractText | 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. |
