Abdominal expiratory activity in the rat brainstem-spinal cord in situ: patterns, origins and implications for respiratory rhythm generation
Abdominal expiratory activity in the rat brainstem-spinal cord in situ: patterns, origins and implications for respiratory rhythm generation
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DOI：
10.1113/jphysiol.2008.167502
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发表时间：
2009-07-15
影响因子：
5.5
通讯作者：
Paton, J. F. R.
中科院分区：
文献类型：
--
作者：
Abdala, A. P. L.;Rybak, I. A.;Paton, J. F. R.
我们研究了呼气时产生的呼吸神经活动。同时记录新生大鼠和幼年大鼠原位腹部（AbN）、膈神经（PN）、舌下神经（HN）和中枢迷走神经的运动神经元活动。在清醒活动期间，低幅度吸气后放电仅出现在AbN运动流出中。在高碳酸血症期间，在PN爆发之前，AbN呼气后（迟-e）活性的表达。双相呼气（双相e）活动伴吸气前（前i）和吸气后（后i）放电仅在先期缺氧或高碳酸血症缺氧时发生。高碳酸（7-10% CO2）时产生的Late-E活性通过脑桥横断或化学抑制后梯形核/腹外侧面旁核（RTN/vlPF）被消除。高血氧症时，AbN晚期e活动与HN期i前放电增强、PN爆发截短相结合，并在吸气时处于静止状态。我们的数据表明，脑桥为额外的神经振荡机制提供了必要的兴奋驱动，该机制仅在高呼吸驱动条件下被激活，以产生指向AbN运动神经元的晚e活动。这种机制可能是由位于RTN/vlPF的神经元引起的，或者后者可能传递其他地方产生的晚e活动。我们假设这种振荡机制不是呼吸中枢模式发生器的必要组成部分，而是在关键代谢条件下激活的防御机制，同时提供强制呼气和降低上呼吸道阻力。讨论了该振荡器与脑干呼吸网络组成部分可能的相互作用。
We studied respiratory neural activity generated during expiration. Motoneuronal activity was recorded simultaneously from abdominal (AbN), phrenic (PN), hypoglossal (HN) and central vagus nerves from neonatal and juvenile rats in situ. During eupnoeic activity, low-amplitude post-inspiratory (post-I) discharge was only present in AbN motor outflow. Expression of AbN late-expiratory (late-E) activity, preceding PN bursts, occurred during hypercapnia. Biphasic expiratory (biphasic-E) activity with pre-inspiratory (pre-I) and post-I discharges occurred only during eucapnic anoxia or hypercapnic anoxia. Late-E activity generated during hypercapnia (7-10% CO2) was abolished with pontine transections or chemical suppression of retrotrapezoid nucleus/ventrolateral parafacial (RTN/vlPF). AbN late-E activity during hypercapnia is coupled with augmented pre-I discharge in HN, truncated PN burst, and was quiescent during inspiration. Our data suggest that the pons provides a necessary excitatory drive to an additional neural oscillatory mechanism that is only activated under conditions of high respiratory drive to generate late-E activity destined for AbN motoneurones. This mechanism may arise from neurons located in the RTN/vlPF or the latter may relay late-E activity generated elsewhere. We hypothesize that this oscillatory mechanism is not a necessary component of the respiratory central pattern generator but constitutes a defensive mechanism activated under critical metabolic conditions to provide forced expiration and reduced upper airway resistance simultaneously. Possible interactions of this oscillator with components of the brainstem respiratory network are discussed.