Peña Fernando, Meza-Andrade Roberto, Páez-Zayas Victor, González-Marín María-Carmen
Departamento de Farmacobiología, Cinvestav-Sede Sur, Calz. de los Tenorios 235, Col. Granjas Coapa, 14330, Mexico, DF, Mexico.
Neurochem Res. 2008 Aug;33(8):1492-500. doi: 10.1007/s11064-008-9616-x. Epub 2008 Feb 14.
During hypoxia the respiratory network produces gasping in vivo and in vitro. To understand the mechanisms involved in such response and to validate in vitro findings, correlative studies are necessary. During perinatal age gasping generation is robust and then declines during postnatal development, possibly due to changes in either the rhythm generator (the pre-Bötzinger complex, PBC) and/or its motor outputs. We tested this hypothesis by recording respiratory response to hypoxia in vivo and in vitro during postnatal development. We found that postnatal age influences: (1) The hypoxia-induced pattern change in the PBC bursts, (2) The coupling between the PBC and the XII nucleus during prolonged hypoxia and (3) The ability of mice to gasp and autoresuscitate from hypoxic conditions. We conclude that the inability of mice to gasp during late postnatal development might be determined by a progressive uncoupling between the respiratory rhythm generator and its motor outputs in hypoxia.
在缺氧期间，呼吸网络在体内和体外都会产生喘息。为了理解这种反应所涉及的机制并验证体外研究结果，进行相关性研究是必要的。在围产期，喘息的产生很强烈，然后在出生后发育过程中下降，这可能是由于节律发生器（前包钦格复合体，PBC）及其运动输出的变化所致。我们通过记录出生后发育过程中体内和体外对缺氧的呼吸反应来检验这一假设。我们发现出生后年龄会影响：（1）缺氧诱导的PBC爆发模式变化，（2）长时间缺氧期间PBC与舌下神经核之间的耦合，以及（3）小鼠在缺氧条件下喘息和自动复苏的能力。我们得出结论，出生后晚期小鼠无法喘息可能是由缺氧时呼吸节律发生器与其运动输出之间的逐渐解耦所决定的。
