The Kölliker-Fuse Nucleus (KF) has been widely investigated for its contribution to "inspiratory off-switch" while more recent studies showed that activation of the Parabrachial Nucleus (PBN) shortened expiratory duration. This study used an adult, in vivo, decerebrate rabbit model to delineate the contribution of each site to inspiratory and expiratory duration through sequential block of glutamatergic excitation with the receptor antagonists 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo[f]quinoxaline-2,3-dione (NBQX) and d(-)-2-amino-5-phosphonopentanoic acid (AP5). Glutamatergic disfacilitation caused large increases in inspiratory and expiratory duration and minor decrease in peak phrenic activity (PPA). Hypoxia only partially reversed respiratory rate depression but PPA was increased to >200 % of control. The contribution of PBN activity to inspiratory and expiratory duration was equal while block of the KF affected inspiratory duration more than expiratory. We conclude that in the in vivo preparation respiratory rate greatly depends on PBN/KF activity, which contributes to the "inspiratory on- "and "off-switch", but is of minor importance for the magnitude of phrenic motor output.

中文翻译：

---

臂旁核/Kölliker-Fuse Complex 的内源性谷氨酸能输入决定呼吸频率。

Kölliker-Fuse Nucleus (KF) 因其对“吸气关闭开关”的贡献而受到广泛研究，而最近的研究表明，臂旁核 (PBN) 的激活缩短了呼气持续时间。本研究使用成人体内去脑兔模型，通过受体拮抗剂 2,3-二羟基-6-硝基-7-氨磺酰苯并连续阻断谷氨酸能激发来描绘每个部位对吸气和呼气持续时间的贡献。 f]quinoxaline-2,3-dione (NBQX) 和 d(-)-2-amino-5-phosphonopentanoic 酸 (AP5)。谷氨酸能障碍导致吸气和呼气持续时间大幅增加，而膈活动峰值 (PPA) 略有下降。缺氧只能部分逆转呼吸频率抑制，但 PPA 增加到>200% 的控制。PBN 活动对吸气和呼气持续时间的贡献相等，而 KF 阻滞对吸气持续时间的影响大于对呼气持续时间的影响。我们得出结论，在体内制剂中，呼吸频率很大程度上取决于 PBN/KF 活性，这有助于“吸气开”和“关开关”，但对膈运动输出的大小并不重要。