首页> 外文期刊>The Journal of Physiology >Abdominal expiratory activity in the rat brainstem-spinal cord in situ: patterns, origins and implications for respiratory rhythm generation.
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Abdominal expiratory activity in the rat brainstem-spinal cord in situ: patterns, origins and implications for respiratory rhythm generation.

机译:大鼠脑干-脊髓原位的腹部呼气活动:模式,起源和呼吸节律产生的影响。

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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% CO(2)) 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.
机译:我们研究了呼气期间产生的呼吸神经活动。同时从新生和幼年大鼠的腹部(AbN),(PN),舌下(HN)和中央迷走神经记录了动神经元活动。在棉麻活动期间,低振幅吸气后(I后)放电仅存在于AbN电机流出中。在PN爆发之前,AbN的呼气晚期(晚期E)活性表达发生在高碳酸血症期间。吸气前(I)和后I放电的双相呼气(biphasic-E)活动仅在正常碳酸血症或高碳酸血症性缺氧期间发生。高碳酸血症(7-10%CO(2))期间产生的Late-E活动被桥脑横断或化学抑制后梯形核/腹侧副界面(RTN / vlPF)废除。高碳酸血症期间的AbN晚期E活性与HN中的pre-I放电增加,PN截短截断有关,并且在吸气期间处于静止状态。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性驱动,该机制仅在高呼吸驱动条件下才被激活,以产生注定为AbN运动神经元的晚期E活性。这种机制可能是由位于RTN / vlPF中的神经元引起的,或者后者可能会中继其他地方产生的Late-E活动。我们假设这种振荡机制不是呼吸中央模式发生器的必要组成部分,而是构成在关键代谢条件下激活的防御机制,以同时提供强制呼气和降低的上呼吸道阻力。讨论了该振荡器与脑干呼吸网络组件的可能相互作用。

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