The Kolliker-Fuse nucleus gates the postinspiratory phase of the respiratory cycle to control inspiratory off-switch and upper airway resistance in rat
The Kolliker-Fuse nucleus gates the postinspiratory phase of the respiratory cycle to control inspiratory off-switch and upper airway resistance in rat
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DOI：
10.1111/j.1460-9568.2006.04981.x
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发表时间：
2006-08-01
影响因子：
3.4
通讯作者：
Herbert, Horst
中科院分区：
文献类型：
--
作者：
Dutschmann, Mathias;Herbert, Horst
脑桥背外侧的病变或药物操作可将呼吸模式转变为呼吸暂停（病理性吸气延长）。呼吸暂停反映了吸气关闭机制 (IOS) 紊乱，导致从吸气到呼气的相变延迟。在完整的条件下，IOS 通过激活呼吸网络内的吸气后 (PI) 神经元不可逆地介导。与此同时，喉前运动神经元群体在 PI 阶段通过短暂的声门收缩来表现 IOS。我们研究了脑桥兴奋（谷氨酸注射）或注射 GABA 受体激动剂（异口疫苗）后暂时性损伤对 PI 池活性强度的影响，PI 池活性是通过呼吸运动输出或灌注脑干制剂中喉部阻力的运动学测量确定的。将谷氨酸微注射到桥脑 Kolliker-Fuse 核 (KF) 的不同部位会引起 PI 运动活动的强直性兴奋或持续的喉部收缩，并伴有呼气相的延长。随后在同一位点进行异鳄梨肽显微注射，消除了 PI 运动或喉缩肌活动，引发呼吸暂停并建立了可变且降低的呼吸频率。总之，我们发现 KF 内特定区域的兴奋或抑制会激活和阻断 PI 活性，从而抑制 IOS。因此，我们得出的结论是，首先，下降的 KF 输入对于呼吸网络内正确模式形成和相位控制所需的 PI 活动至关重要，至少在没有肺牵张受体活动的情况下是如此；其次，KF 包含大量的喉部 PI 前运动神经元，这些神经元可能在反射控制和发声期间对上气道阻力的调节中发挥关键作用。
Lesion or pharmacological manipulation of the dorsolateral pons can transform the breathing pattern to apneusis (pathological prolonged inspiration). Apneusis reflects a disturbed inspiratory off-switch mechanism (IOS) leading to a delayed phase transition from inspiration to expiration. Under intact conditions the IOS is irreversibly mediated via activation of postinspiratory (PI) neurons within the respiratory network. In parallel, populations of laryngeal premotoneurons manifest the IOS by a brief glottal constriction during the PI phase. We investigated effects of pontine excitation (glutamate injection) or temporary lesion after injection of a GABA-receptor agonist (isoguvacine) on the strength of PI-pool activity determined from respiratory motor outputs or kinesiological measurements of laryngeal resistance in a perfused brainstem preparation. Glutamate microinjections into distinct parts of the pontine Kolliker-Fuse nucleus (KF) evoked a tonic excitation of PI-motor activity or sustained laryngeal constriction accompanied by prolongation of the expiratory phase. Subsequent isoguvacine microinjections at the same loci abolished PI-motor or laryngeal constrictor activity, triggered apneusis and established a variable and decreased breathing frequency. In summary, we revealed that excitation or inhibition of defined areas within the KF activated and blocked PI activity and, consequently, IOS. Therefore, we conclude, first, that descending KF inputs are essential to gate PI activity required for a proper pattern formation and phase control within the respiratory network, at least during absence of pulmonary stretch receptor activity and, secondly, that the KF contains large numbers of laryngeal PI premotor neurons that might have a key role in the regulation of upper airway resistance during reflex control and vocalization.