Department of Pediatrics, Université Laval, Québec, QC, Canada.
Institut Universitaire de Cardiologie et de Pneumologie de Québec, Québec, QC, Canada.
Adv Exp Med Biol. 2018;1071:75-82. doi: 10.1007/978-3-319-91137-3_9.
During vertebrate development, the neural networks underlying air-breathing undergo changes in connectivity and functionality, allowing lung ventilation to emerge. Yet, the factors regulating development of these critical homeostatic networks remain unresolved. In amphibians, air-breathing occurs sporadically prior to metamorphosis. However, in tadpoles of Lithobates catesbeianus (American bullfrog), hypoxia stimulates gill and lung ventilation during early development. Because accelerated metamorphosis is a useful strategy to escape deterioration of the milieu, we hypothesized that central hypoxia would elicit long-term expression of the lung motor command for air breathing in pre-metamorphic tadpoles (TK stages VI-XIII). To do this, we recorded respiratory activity from cranial nerves V and VII in isolated brainstems before, during, and up to 2 h after exposure to 15 min of mild (PwO range: 114-152 Torr) or moderate (PwO range: 38-76 Torr) hypoxia. To test for stage-dependent effects, data were compared between early (VI-IX) and mid (X-XIII) stages. Early stages responded strongly during moderate hypoxia with increased lung burst frequency (167%). Mild and moderate hypoxia increased lung burst frequency during the 2 h re-oxygenation period in early stage brainstems (136%, 497%, respectively), but produced only marginal effects on mid stage brainstems (39%, 31%, respectively). In contrast, hypoxia was not an important factor controlling fictive buccal burst frequency, which drives continuous gill ventilation in tadpoles prior to metamorphosis (all stages showed <25% increase). These preliminary results suggest that central hypoxia elicits long-term increases in lung burst frequency in a severity- and stage-dependent manner.
在脊椎动物发育过程中，呼吸空气的神经网络在连接性和功能上发生变化，从而使肺通气得以出现。然而，调节这些关键稳态网络发育的因素仍未得到解决。在两栖动物中，呼吸空气的现象在变态之前偶尔发生。然而，在 Lithobates catesbeianus（美洲牛蛙）的蝌蚪中，缺氧会在早期发育过程中刺激鳃和肺的通气。由于加速变态是逃避环境恶化的有用策略，我们假设中枢缺氧会在预变态蝌蚪（TK 阶段 VI-XIII）中引发长期表达用于空气呼吸的肺运动命令。为此，我们在暴露于 15 分钟轻度（PwO 范围：114-152 托）或中度（PwO 范围：38-76 托）缺氧之前、期间和之后，从孤立的脑干中记录颅神经 V 和 VII 的呼吸活动。为了测试阶段依赖性影响，我们将早期（VI-IX）和中期（X-XIII）阶段的数据进行了比较。在中度缺氧期间，早期阶段反应强烈，肺爆发频率增加（167%）。轻度和中度缺氧在早期脑干的 2 小时再氧合期间增加了肺爆发频率（分别为 136%和 497%），但对中期脑干仅产生了微小的影响（分别为 39%和 31%）。相比之下，缺氧不是控制在变态前驱动蝌蚪连续鳃通气的虚构颊部爆发频率的重要因素（所有阶段的增加都<25%）。这些初步结果表明，中枢缺氧以严重程度和阶段依赖性的方式引起肺爆发频率的长期增加。
