Attenuation of phrenic motor discharge by phrenic nerve afferents

Speck, D. F.; Revelette, W. R.

doi:10.1152/jappl.1987.62.3.941

Cited by 55 publications

(37 citation statements)

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“…However, in this study, we examined the effect of 8-OH-DPAT at the level of the cervical spinal cord, and the diaphragm is essentially devoid of all group II sensory afferents. In addition, most phrenic afferent-supraspinal respiratory reflexes result in excitation of respiratory output (28,29), whereas inhibitory mechanisms are mediated at a spinal level (21,22,30). This suggests that the role of 5HT1A agonists in increasing phrenic activity that was observed in this study must be mediated by something other than group II afferents.…”

Section: Dorsal Horn Afferent-supraspinal-mediated Respiratory Reflexesmentioning

confidence: 58%

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Spinal Activation of Serotonin 1A Receptors Enhances Latent Respiratory Activity After Spinal Cord Injury

Zimmer

Goshgarian

2006

The Journal of Spinal Cord Medicine

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Background/Objective: Hemisection of the cervical spinal cord results in paralysis of the ipsilateral hemidiaphragm. Removal of sensory feedback through cervical dorsal rhizotomy activates latent respiratory motor pathways and restores hemidiaphragm function. Because systemic administration of serotonin 1A receptor (5HT1A) agonists reversed the altered breathing patterns after spinal cord injury (SCI), we predicted that 5HT1A receptor activation after SCI (C2) would activate latent crossed motor pathways. Furthermore, because 5HT1A receptors are heavily localized to dorsal horn neurons, we predicted that spinal administration of 5HT1A agonists should also activate latent motor pathways.Methods: Hemisection of the C2 spinal cord was performed 24 to 48 hours, 1 week, or 16 weeks before experimentation. Bilateral phrenic nerve activity was recorded in anesthetized, vagotomized, paralyzed Sprague-Dawley rats, and 8-OH-DPAT (5HT1A agonist) was applied to the dorsal aspect of the cervical spinal cord (C3-C7) or injected systemically.Results: Systemic administration of 8-OH-DPAT led to a significant increase in phrenic frequency and amplitude, whereas direct application to the spinal cord increased phrenic amplitude alone. Both systemic and spinal administration of 8-OH-DPAT consistently activated latent crossed phrenic activity. 8-OH-DPAT induced a greater respiratory response in spinal injured rats compared with controls. Conclusion:The increase in crossed phrenic output after application of 8-OH-DPAT to the spinal cord suggests that dorsal horn inputs, respiratory and/or nonrespiratory, may inhibit phrenic motor output, especially after SCI. These findings support the idea that the administration of 5HT1A agonists may be a beneficial therapy in enhancing respiratory neural output in patients with SCI.

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Section: Dorsal Horn Afferent-supraspinal-mediated Respiratory Reflexesmentioning

confidence: 58%

“…Within the respiratory system, sensory afferent stimulation during inspiration results in the inhibition of phrenic motor output (21): the phrenic-to phrenic inhibitory reflex. This reflex is a segmental spinal reflex that is most likely mediated through nonrespiratory interneurons of the dorsal spinal cord (22,23).…”

Section: Introductionmentioning

confidence: 99%

Spinal Activation of Serotonin 1A Receptors Enhances Latent Respiratory Activity After Spinal Cord Injury

Zimmer

Goshgarian

2006

The Journal of Spinal Cord Medicine

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“…In the respiratory system, stimulation of cervical dorsal afferents during the inspiratory phase results in the inhibition of phrenic motor output (85). This reflex is a segmental spinal reflex that is most likely mediated through nonrespiratory interneurons located in the dorsal horn of the spinal cord (86,87).…”

Section: Disinhibition Of Phrenic Motor Neuronsmentioning

confidence: 99%

Effect of Spinal Cord Injury on the Respiratory System: Basic Research and Current Clinical Treatment Options

Zimmer

Nantwi

Goshgarian

2007

The Journal of Spinal Cord Medicine

154

126

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Summary: Spinal cord injury (SCI) often leads to an impairment of the respiratory system. The more rostral the level of injury, the more likely the injury will affect ventilation. In fact, respiratory insufficiency is the number one cause of mortality and morbidity after SCI. This review highlights the progress that has been made in basic and clinical research, while noting the gaps in our knowledge. Basic research has focused on a hemisection injury model to examine methods aimed at improving respiratory function after SCI, but contusion injury models have also been used. Increasing synaptic plasticity, strengthening spared axonal pathways, and the disinhibition of phrenic motor neurons all result in the activation of a latent respiratory motor pathway that restores function to a previously paralyzed hemidiaphragm in animal models. Human clinical studies have revealed that respiratory function is negatively impacted by SCI. Respiratory muscle training regimens may improve inspiratory function after SCI, but more thorough and carefully designed studies are needed to adequately address this issue. Phrenic nerve and diaphragm pacing are options available to wean patients from standard mechanical ventilation. The techniques aimed at improving respiratory function in humans with SCI have both pros and cons, but having more options available to the clinician allows for more individualized treatment, resulting in better patient care. Despite significant progress in both basic and clinical research, there is still a significant gap in our understanding of the effect of SCI on the respiratory system.

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“…Indeed, afferent fibers make up 40 -45% of the phrenic nerve (33,34), and these afferents project to spinal (25,61) and supraspinal (12,62) structures. Although a direct role of phrenic afferents in modulating the excitability of phrenic motoneurons has not been definitively shown, there is indirect evidence suggesting that afferents can reflexly affect the phrenic motor drive (15,23,29,55,63).…”

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confidence: 99%

Phrenicotomy alters phrenic long-term facilitation following intermittent hypoxia in anesthetized rats

Sandhu

Lee

Fregosi

et al. 2010

Journal of Applied Physiology

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Sandhu MS, Lee KZ, Fregosi RF, Fuller DD. Phrenicotomy alters phrenic long-term facilitation following intermittent hypoxia in anesthetized rats. J Appl Physiol 109: 279 -287, 2010. First published April 15, 2010 doi:10.1152/japplphysiol.01422.2009 can induce a persistent increase in neural drive to the respiratory muscles known as long-term facilitation (LTF). LTF of phrenic inspiratory activity is often studied in anesthetized animals after phrenicotomy (PhrX), with subsequent recordings being made from the proximal stump of the phrenic nerve. However, severing afferent and efferent axons in the phrenic nerve has the potential to alter the excitability of phrenic motoneurons, which has been hypothesized to be an important determinant of phrenic LTF. Here we test the hypothesis that acute PhrX influences immediate and long-term phrenic motor responses to hypoxia. Phrenic neurograms were recorded in anesthetized, ventilated, and vagotomized adult male rats with intact phrenic nerves or bilateral PhrX. Data were obtained before (i.e., baseline), during, and after three 5-min bouts of isocapnic hypoxia. Inspiratory burst amplitude during hypoxia (%baseline) was greater in PhrX than in phrenic nerve-intact rats (P Ͻ 0.001). Similarly, burst amplitude 55 min after IH was greater in PhrX than in phrenic nerve-intact rats (175 Ϯ 9 vs. 126 Ϯ 8% baseline, P Ͻ 0.001).In separate experiments, phrenic bursting was recorded before and after PhrX in the same animal. Afferent bursting that was clearly observable in phase with lung deflation was immediately abolished by PhrX. The PhrX procedure also induced a form of facilitation as inspiratory burst amplitude was increased at 30 min post-PhrX (P ϭ 0.01 vs. pre-PhrX). We conclude that, after PhrX, axotomy of phrenic motoneurons and, possibly, removal of phrenic afferents result in increased phrenic motoneuron excitability and enhanced LTF following IH. axotomy; phrenic motoneurons; plasticity EXPOSURE TO INTERMITTENT HYPOXIA (IH) over short periods (e.g., minutes to hours) can evoke a persistent increase in respiratory motor output, termed long-term facilitation (LTF) (35,48,50). LTF has been observed in awake (26, 35) and sleeping humans (53) and in a wide range of animal species (22,46,48). The mechanisms underlying LTF have been studied extensively over the last 10 -15 years, primarily in anesthetized animals (reviewed in Refs. 42,49,50). In anesthetized animals, LTF is typically manifest as an increase in the inspiratory burst amplitude of phrenic (19) and/or hypoglossal (XII) extracellular nerve recordings (20). Recordings of in vivo (19) and in vitro (10) respiratory motor LTF are typically made from cut respiratory muscle nerves. More specifically, the phrenic and/or XII nerves are cut, and subsequent extracellular recordings are made from the central end of the nerve. This procedure can provide stability to the neurophysiological recording procedures, particularly when a dorsal surgical approach is used, but also has the potential to alter respiratory motor output and...

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Attenuation of phrenic motor discharge by phrenic nerve afferents

Cited by 55 publications

References 0 publications

Spinal Activation of Serotonin 1A Receptors Enhances Latent Respiratory Activity After Spinal Cord Injury

Spinal Activation of Serotonin 1A Receptors Enhances Latent Respiratory Activity After Spinal Cord Injury

Effect of Spinal Cord Injury on the Respiratory System: Basic Research and Current Clinical Treatment Options

Phrenicotomy alters phrenic long-term facilitation following intermittent hypoxia in anesthetized rats

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