Analysis of postinspiratory activity of phrenic motoneurons with chemical and vagal reflexes

Prabhakar, Nanduri R.; Mitra, J.; Overholt, Jeffrey L.; Cherniack, Neil S.

doi:10.1152/jappl.1986.61.4.1499

Cited by 25 publications

(15 citation statements)

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“…Early-I PMNs show more action potential spikes per breath, and have a longer overall discharge duration compared to Late-I cells. However, the mean discharge frequency and the interspike interval are similar between Early-I and Late-I PMNs (Hilaire et al, 1983; Hwang and St John, 1993; Kong and Berger, 1986; Lee et al, 1990; Lee et al, 2009; Prabhakar et al, 1986; St John and Bartlett, 1979, 1981). A few studies have reported that Early-I, but not Late-I PMNs can continue bursting during the post-inspiratory period (Kong and Berger, 1986; Prabhakar et al, 1986).…”

Section: Pmn Discharge Patternsmentioning

confidence: 90%

“…Hypoxia, as expected, increases the discharge frequency of both Early-I and Late-I PMNs and recruit previously silent cells. Late-I PMNs also show an earlier burst onset during hypoxic stimulation (Lee et al, 1990; Lee et al, 2009; Prabhakar et al, 1986; St John and Bartlett, 1979). We recently observed that hypoxia induces differential responses in Early-I vs. Late-I PMNs (Lee et al, 2009).…”

Section: Pmn Discharge Patternsmentioning

confidence: 96%

“…This study demonstrated that discharge frequency of the PMN was progressively enhanced when end-tidal CO 2 was increased above the CO 2 PMN recruitment threshold. Although the discharge frequency of all PMNs is increased by hypercapnia, differential responses of Early-I vs. Late-I cells have been described in both cat and rat (Kong and Berger, 1986; Prabhakar et al, 1986; St John and Bartlett, 1979). These studies indicated that hypercapnia results in an earlier discharge onset of Late-I PMN with no change in Early-I PMN burst onset.…”

Section: Pmn Discharge Patternsmentioning

confidence: 99%

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Neural control of phrenic motoneuron discharge

Lee

Fuller

2011

Respiratory Physiology & Neurobiology

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Phrenic motoneurons (PMNs) provide a synaptic relay between bulbospinal respiratory pathways and the diaphragm muscle. PMNs also receive propriospinal inputs, although the functional role of these interneuronal projections has not been established. Here we review the literature regarding PMN discharge patterns during breathing and the potential mechanisms that underlie PMN recruitment. Anatomical and neurophysiological studies indicate that PMNs form a heterogeneous pool, with respiratory-related PMN discharge and recruitment patterns likely determined by a balance between intrinsic MN properties and extrinsic synaptic inputs. We also review the limited literature regarding PMN bursting during respiratory plasticity. Differential recruitment or rate modulation of PMN subtypes may underlie phrenic motor plasticity following neural injury and/or respiratory stimulation; however this possibility remains relatively unexplored.

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Section: Pmn Discharge Patternsmentioning

confidence: 90%

Section: Pmn Discharge Patternsmentioning

confidence: 96%

Section: Pmn Discharge Patternsmentioning

confidence: 99%

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Neural control of phrenic motoneuron discharge

Lee

Fuller

2011

Respiratory Physiology & Neurobiology

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“…Next, force generated at 40 H Z by direct muscle stimulation (P 40 M) was measured, to obtain a measure of the quality of the preparations. A stimulation frequency of 40 H Z was chosen because diaphragm motor units typically fire at frequencies ranging from 20 to 40 H Z when breathing is stimulated by hypoxia 35, 44. Subsequently, the perfusion of the tissue bath was either maintained at hyperoxia (95%O 2 –5%CO 2 ) or switched to hypoxia (95%N 2 –5%CO 2 ); the Krebs solution was replaced by the experimental Krebs solutions.…”

Section: Methodsmentioning

confidence: 99%

Nitric oxide modulates neuromuscular transmission during hypoxia in rat diaphragm

Zhu¹,

Heunks²,

Ennen³

et al. 2005

Muscle and Nerve

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Hypoxia impairs neuromuscular transmission in the rat diaphragm. In previous studies, we have shown that nitric oxide (NO) plays a role in force modulation of the diaphragm under hypoxic conditions. The role of NO, a neurotransmitter, on neurotransmission in skeletal muscle under hypoxic conditions is unknown. The effects of the NO synthase (NOS) inhibitor nomega-nitro-L-arginine (L-NNA, 1 mM) and the NO donor spermine NONOate (Sp-NO, 1 mM) were evaluated on neurotransmission failure during nonfatiguing and fatiguing contractions of the rat diaphragm under hypoxic (PO 2 ϳ 5.8 kPa) and hyperoxic conditions (PO 2 ϳ 64.0 kPa). Hypoxia impaired force generated by both muscle stimulation at 40 HZ (P 40 M) and by nerve stimulation at 40 HZ (P 40 N). The effect of hypoxia in the latter was more pronounced. L-NNA increased P 40 N whereas Sp-NO decreased P 40 N during hypoxia. In contrast, neither L-NNA nor Sp-NO affected P 40 N during hyperoxia. L-NNA only slightly reduced neurotransmission failure during fatiguing contractions under hyperoxic conditions. Consequently, neurotransmission failure assessed by comparing force loss during repetitive nerve simulation and superimposed direct muscle stimulation was more pronounced in hypoxia, which was alleviated by L-NNA and aggravated by Sp-NO. These data provide insight in the underlying mechanisms of hypoxia-induced neurotransmission failure. This is important as respiratory muscle failure may result from hypoxia in vivo. Respiratory muscle fatigue, especially that of the diaphragm, is a possible contributor to the development of respiratory failure-for instance, in patients with chronic obstructive pulmonary disease (COPD). 24 Diaphragm fatigue may be the result of a failure of the muscle tissue itself to generate force (contractile fatigue) or failure in neuromuscular transmission. 3 In vitro studies indicate that the contribution of neurotransmission failure to muscle fatigue ranges from 18% 17 to as much as 75%. 1 The importance of neuromuscular transmission failure in the development of respiratory failure has also been demonstrated in intact animals. 5 Hypoxia, a common feature in several respiratory diseases including COPD, adult respiratory distress syndrome, and pneumonia, impairs neuromuscular transmission in the rat diaphragm. 4 However, little is known about the underlying mechanisms of hypoxiainduced neurotransmission failure in the respiratory muscles. In skeletal muscle, nitric oxide (NO) plays a role in the regulation of neural transmission. 31,47 Skeletal muscle is a major source for NO in the body 32 and neuronal NO synthase (nNOS) is present in high concentrations at the postsynaptic surface of the neuromuscular junction of both fast-and slowtwitch fibers. 7,21 Furthermore, NO appears to influence acetylcholine release from presynaptic terminals in several types of neuromuscular junction models, including skeletal muscle. 31,37 We have previously shown that hypoxia-induced impairment in rat diaphragm contractile performance is associated with el...

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“…hypercapnia and hypoxia) specifically induced an earlier discharge in Late‐I but not Early‐I phrenic motoneurons (Kong & Berger, ; Prabhakar et al . ; Lee et al . ).…”

Section: Introductionmentioning

confidence: 99%

Phrenic motor outputs in response to bronchopulmonary C‐fibre activation following chronic cervical spinal cord injury

Lee

2016

The Journal of Physiology

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Cervical spinal injury interrupts bulbospinal pathways and results in cessation of phrenic bursting ipsilateral to the lesion. The ipsilateral phrenic activity can partially recover over weeks to months following injury due to the activation of latent crossed spinal pathways and exhibits a greater capacity to increase activity during respiratory challenges than the contralateral phrenic nerve. However, whether the bilateral phrenic nerves demonstrate differential responses to respiratory inhibitory inputs is unclear. Accordingly, the present study examined bilateral phrenic bursting in response to capsaicin-induced pulmonary chemoreflexes, a robust respiratory inhibitory stimulus. Bilateral phrenic nerve activity was recorded in anaesthetized and mechanically ventilated adult rats at 8-9 weeks after C2 hemisection (C2Hx) or C2 laminectomy. Intra-jugular capsaicin (1.5 μg kg ) injection was performed to activate the bronchopulmonary C-fibres to evoke pulmonary chemoreflexes. The present results indicate that capsaicin-induced prolongation of expiratory duration was significantly attenuated in C2Hx animals. However, ipsilateral phrenic activity was robustly reduced after capsaicin treatment compared to uninjured animals. Single phrenic fibre recording experiments demonstrated that C2Hx animals had a higher proportion of late-inspiratory phrenic motoneurons that were relatively sensitive to capsaicin treatment compared to early-inspiratory phrenic motoneurons. Moreover, late-inspiratory phrenic motoneurons in C2Hx animals had a weaker discharge frequency and slower recovery time than uninjured animals. These results suggest bilateral phrenic nerves differentially respond to bronchopulmonary C-fibre activation following unilateral cervical hemisection, and the severe inhibition of phrenic bursting is due to a shift in the discharge pattern of phrenic motoneurons.

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Analysis of postinspiratory activity of phrenic motoneurons with chemical and vagal reflexes

Cited by 25 publications

References 0 publications

Neural control of phrenic motoneuron discharge

Neural control of phrenic motoneuron discharge

Nitric oxide modulates neuromuscular transmission during hypoxia in rat diaphragm

Phrenic motor outputs in response to bronchopulmonary C‐fibre activation following chronic cervical spinal cord injury

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