Department of Neuroscience, Baylor College of Medicine, Houston, United States.
Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital, Houston, United States.
Elife. 2018 Jul 4;7:e38455. doi: 10.7554/eLife.38455.
-null mice die at birth from respiratory failure, but the precise cause has remained elusive. Loss of from various components of the respiratory circuitry (e.g. the retrotrapezoid nucleus (RTN)) has so far produced at most 50% neonatal lethality. To identify other -lineage neurons that contribute to postnatal survival, we examined parabrachial complex neurons derived from the rostral rhombic lip (rRL) and found that they are activated during respiratory chemochallenges. -deletion from the rRL does not affect survival, but causes apneas and respiratory depression during hypoxia, likely due to loss of projections to the preBötzinger Complex and RTN. thus promotes the development of the neural circuits governing hypoxic (rRL) and hypercapnic (RTN) chemoresponses, and combined loss of from these regions causes fully penetrant neonatal lethality. This work underscores the importance of modulating respiratory rhythms in response to chemosensory information during early postnatal life.
null 小鼠会在出生时因呼吸衰竭而死亡，但确切原因仍未可知。迄今为止，呼吸回路的各种成分（如梯形核后区（RTN））的缺失最多导致 50%的新生仔鼠致死。为了鉴定其他对出生后存活有贡献的神经前体细胞，我们检查了源自颅侧菱形唇（rRL）的臂旁复合体神经元，发现它们在呼吸化学刺激期间被激活。rRL 中的缺失并不影响存活，但会导致缺氧时的呼吸暂停和呼吸抑制，这可能是由于向 PreBötzinger 复合体和 RTN 的投射缺失所致。因此，它促进了调节缺氧（rRL）和高碳酸血症（RTN）化学反应的神经回路的发育，而这些区域中 的联合缺失会导致完全穿透性的新生仔鼠致死。这项工作强调了在出生后早期响应化学感觉信息来调节呼吸节律的重要性。
