1. Role of the Kölliker-Fuse/parabrachial complex in the generation of postinspiratory vagal and sympathetic nerve activities and their recruitment by hypoxemic stimuli in the rat.
- Author
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Toor RUAS, Burke PGR, Dempsey B, Sun QJ, Hildreth CM, Phillips JK, and McMullan S
- Subjects
- Animals, Male, Rats, Parabrachial Nucleus physiology, Parabrachial Nucleus drug effects, Rats, Sprague-Dawley, Respiration, Phrenic Nerve physiology, Phrenic Nerve drug effects, GABA-A Receptor Agonists pharmacology, Isonicotinic Acids, Vagus Nerve physiology, Vagus Nerve drug effects, Hypoxia physiopathology, Kolliker-Fuse Nucleus physiology, Sympathetic Nervous System physiology, Sympathetic Nervous System drug effects, Sympathetic Nervous System physiopathology
- Abstract
In the rat, the activity of laryngeal adductor muscles, the crural diaphragm, and sympathetic vasomotor neurons is entrained to the postinspiratory (post-I) phase of the respiratory cycle, a mechanism thought to enhance cardiorespiratory efficiency. The identity of the central neurons responsible for transmitting respiratory activity to these outputs remains unresolved. Here we explore the contribution of the Kölliker-Fuse/parabrachial nuclei (KF-PBN) in the generation of post-I activity in vagal and sympathetic outputs under steady-state conditions and during acute hypoxemia, a condition that potently recruits post-I activity. In artificially ventilated, vagotomized, and urethane-anesthetized rats, bilateral KF-PBN inhibition by microinjection of the GABA
A receptor agonist isoguvacine evoked stereotypical responses on respiratory pattern, characterized by a reduction in phrenic nerve burst amplitude, a modest lengthening of inspiratory time, and an increase in breath-to-breath variability, while post-I vagal nerve activity was abolished and post-I sympathetic nerve activity diminished. During acute hypoxemia, KF-PBN inhibition attenuated tachypneic responses and completely abolished post-I vagal activity while preserving respiratory-sympathetic coupling. Furthermore, KF-PBN inhibition disrupted the decline in respiratory frequency that normally follows resumption of oxygenation. These findings suggest that the KF-PBN is a critical hub for the distribution of post-I activities to vagal and sympathetic outputs and is an important contributor to the dynamic adjustments to respiratory patterns that occur in response to acute hypoxia. Although KF-PBN appears essential for post-I vagal activity, it only partially contributes to post-I sympathetic nerve activity, suggesting the contribution of multiple neural pathways to respiratory-sympathetic coupling. NEW & NOTEWORTHY Inhibition of neurons in the pontine Kölliker-Fuse/parabrachial complex (KF-PBN) differentially inhibited postinspiratory (post-I) activity in vagal and sympathetic outputs. The strong recruitment of post-I vagal activity that occurs in response to hypoxemia is selectively abolished by KF-PBN inhibition. This suggests that 1 ) post-I activity in vagal and sympathetic outputs may be generated by partially independent mechanisms and 2 ) neurons in the KF-PBN are a preeminent source of drive for the generation of eupneic post-I activity.- Published
- 2024
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