Modification by chemical stimuli of temporal difference in the onset of inspiratory activity between vagal (superior laryngeal) or hypoglossal and phrenic nerves of the rat.

Fukuda, Yasuichiro; Honda, Yoshiyuki

doi:10.2170/jjphysiol.38.309

Cited by 14 publications

(17 citation statements)

References 14 publications

(12 reference statements)

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“…Interestingly, this delay has been shown to increase during hypercapnia (Fukuda and Honda 1988). In Fig.…”

Section: Late-e Activity and Temporal Relationships Between Pn And Hnmentioning

confidence: 75%

“…The onset of the PN inspiratory bursts under normal conditions is usually delayed (by ϳ100 ms) relative to the HN bursts (Fukuda and Honda 1988;Leiter and St.-John 2004;Peever et al 2002;Rybak et al 2007;). Interestingly, this delay has been shown to increase during hypercapnia (Fukuda and Honda 1988).…”

Section: Late-e Activity and Temporal Relationships Between Pn And Hnmentioning

confidence: 99%

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Late-Expiratory Activity: Emergence and Interactions With the Respiratory CPG

Molkov

Abdala

Bacak

et al. 2010

Journal of Neurophysiology

199

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The respiratory rhythm and motor pattern are hypothesized to be generated by a brain stem respiratory network with a rhythmogenic core consisting of neural populations interacting within and between the pre-Bötzinger (pre-BötC) and Bötzinger (BötC) complexes and controlled by drives from other brain stem compartments. Our previous large-scale computational model reproduced the behavior of this network under many different conditions but did not consider neural oscillations that were proposed to emerge within the retrotrapezoid nucleus/parafacial respiratory group (RTN/pFRG) and drive preinspiratory (or late-expiratory, late-E) discharges in the abdominal motor output. Here we extend the analysis of our previously published data and consider new data on the generation of abdominal late-E activity as the basis for extending our computational model. The extended model incorporates an additional late-E population in RTN/pFRG, representing a source of late-E oscillatory activity. In the proposed model, under normal metabolic conditions, this RTN/pFRG oscillator is inhibited by BötC/pre-BötC circuits, and the late-E oscillations can be released by either hypercapnia-evoked activation of RTN/pFRG or by hypoxia-dependent suppression of RTN/pFRG inhibition by BötC/pre-BötC. The proposed interactions between BötC/pre-BötC and RTN/pFRG allow the model to reproduce several experimentally observed behaviors, including quantal acceleration of abdominal late-E oscillations with progressive hypercapnia and quantal slowing of phrenic activity with progressive suppression of pre-BötC excitability, as well as to predict a release of late-E oscillations by disinhibition of RTN/pFRG under normal conditions. The extended model proposes mechanistic explanations for the emergence of RTN/pFRG oscillations and their interaction with the brain stem respiratory network.

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“…Interestingly, this delay has been shown to increase during hypercapnia (Fukuda and Honda 1988). In Fig.…”

Section: Late-e Activity and Temporal Relationships Between Pn And Hnmentioning

confidence: 75%

Section: Late-e Activity and Temporal Relationships Between Pn And Hnmentioning

confidence: 99%

Late-Expiratory Activity: Emergence and Interactions With the Respiratory CPG

Molkov

Abdala

Bacak

et al. 2010

Journal of Neurophysiology

199

View full text Add to dashboard Cite

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“…The HVD in the vagotomized and spontaneously breathing rat is also produced by a marked prolongation of TE (MARUYAMA et al, 1986). Our previous report on the vagotomized and artificially ventilated rat showed that a reduction in f during hypoxia was caused by retardation of transition from expiration to inspiration (or onset of inspiratory activity) but not by alteration of inspiratory off-switch (FUKUDA and HONDA, 1988). This finding indicates that the later (or second) phase of expiration rather than early expiratory (postinspiratory) phase (RICHTER, 1982) is the major site of hypoxic deterioration in the rat.…”

Section: Discussionmentioning

confidence: 90%

“…If there were different sensitivities to hypoxia among different components of respiratory regulation processes, they would appear as selective changes in breathing patterns such as tidal volume, respiratory frequency or timing. This possibility has been partly deduced from our previous observation that the onset of inspiratory activity is preferentially deteriorated during asphyxia with maintained phrenic inspiratory discharges in the vagotomized and artificially ventilated rat (FUKUDA and HONDA, 1988). The present study addresses general issues regarding the nature of HVD with an emphasis on the central inhibitory actions of hypoxia on processes for respiratory regulation and their offset by peripheral chemoreceptor afferents.…”

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confidence: 86%

Differential sensitivity to hypoxic inhibition of respiratory processes in the anesthetized rat.

1989

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To estimate the sensitivity to hypoxic inhibition of various regulatory processes for respiration, changes in breathing pattern during hypoxic ventilatory depression (HVD) were analyzed in the halothaneanesthetized spontaneously breathing rat using a "progressive isocapnic hypoxia test." In the carotid sinus nerve (CSN) intact rats, ventilatory augmentation was followed by depression due to reduction in respiratory frequency (f) at end-tidal Po2(PETo2) levels below 50-60 mmHg despite increased afferent activities from the carotid chemoreceptors. After CSN section, ventilation was progressively depressed at PETo2 lower than normoxic level with simultaneous decreases of f and tidal volume. An increase in C02 stimulus or the prevention of arterial hypotension during hypoxia by infusing a vasoconstrictor agent (phenylephrine) inhibited the occurrence of ventilatory depression in both the CSN intact and denervated animals. In all cases studied, the reduction in f resulted mainly from the prolongation of expiratory time (TE). The results suggest that in the anesthetized rat the effect of respiratory stimulation from carotid chemoreceptor afferents becomes inadequate to offset the prolongation of TE due to the central hypoxia at lower PETo2, and that the neural process for regulating TE is the major site of deterioration during central hypoxic inhibition. Roles of C02 stimulus and systemic circulatory conditions in the generation of HVD were also discussed.

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“…There is a precedent for respiratory-related discharge in the HN to respond to physiological perturbations similarly to other UAW motor nerves. For example, changes in Pre-I neural discharge in response to hypocapnia and vagotomy are similar for the SLN and the HN (7,8). In addition, I discharges in the HN and FN commence earlier in response to UAW negative pressure (43).…”

mentioning

confidence: 99%

Uncoupling of upper airway motor activity from phrenic bursting by positive end-expired pressure in the rat

Lee¹,

Fuller²,

Tung³

et al. 2007

Journal of Applied Physiology

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Lee K-Z, Fuller DD, Tung L-C, Lu I-J, Ku L-C, Hwang J-C. Uncoupling of upper airway motor activity from phrenic bursting by positive end-expired pressure in the rat. J Appl Physiol 102: [878][879][880][881][882][883][884][885][886][887][888][889] 2007. First published November 2, 2006; doi:10.1152/japplphysiol.00934.2006.-Phasic bursting in the hypoglossal nerve can be uncoupled from phrenic bursting by application of positive end-expired pressure (PEEP). We wished to determine whether similar uncoupling can also be induced in other respiratory-modulated upper airway (UAW) motor outputs. Discharge of the facial, hypoglossal, superior laryngeal, recurrent laryngeal, and phrenic nerves was recorded in anesthetized, ventilated rats during stepwise changes in PEEP with a normocapnic, hyperoxic background. Application of 3-to 6-cmH 2O PEEP caused the onset inspiratory (I) UAW nerve bursting to precede the phrenic burst but did not uncouple bursting. In contrast, application of 9-to 12-cmH2O PEEP uncoupled UAW neurograms such that rhythmic bursting occurred during periods of phrenic quiescence. Single-fiber recording experiments were conducted to determine whether a specific population of UAW motoneurons is recruited during uncoupled bursting. The data indicate that expiratory-inspiratory (EI) motoneurons remained active, while I motoneurons did not fire during uncoupled UAW bursting. Finally, we examined the relationship between motoneuron discharge rate and PEEP during coupled UAW and phrenic bursting. EI discharge rate was linearly related to PEEP during preinspiration, but showed no relationship to PEEP during inspiration. Our results demonstrate that multiple UAW motor outputs can be uncoupled from phrenic bursting, and this response is associated with bursting of EI nerve fibers. The relationship between PEEP and EI motoneuron discharge rate differs during preinspiratory and I periods; this may indicate that bursting during these phases of the respiratory cycle is controlled by distinct neuronal outputs. uncoupled activity; motoneurons; expiratory-inspiratory; preinspiratory THE MAMMALIAN UPPER AIRWAY (UAW) consists of the airflow passages extending from the trachea to the external nares and is thus composed of the nasal cavity, pharynx, and larynx (34). The compliance and geometry of this region are influenced by a number of skeletal muscles. Among them are the alae nasi, tongue, and laryngeal muscles, which are innervated by the facial (FN), hypoglossal (HN) and superior (SLN), and recurrent laryngeal nerves (RLN), respectively (1,26,41).Many studies have shown that the inspiratory (I) discharge of the HN precedes the phrenic I burst (5,6,13,17,23,33). This preinspiratory (Pre-I) activity has been suggested to benefit UAW patency by dilating and stiffening the UAW before the onset of I airflow (30). Similar to the HN, the onset of FN, SLN, and RLN I bursting occurs before the onset of phrenic bursting (16,25).The respiratory-related discharge of the UAW muscles is influenced by various chemical and mechanical ...

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Modification by chemical stimuli of temporal difference in the onset of inspiratory activity between vagal (superior laryngeal) or hypoglossal and phrenic nerves of the rat.

Cited by 14 publications

References 14 publications

Late-Expiratory Activity: Emergence and Interactions With the Respiratory CPG

Late-Expiratory Activity: Emergence and Interactions With the Respiratory CPG

Differential sensitivity to hypoxic inhibition of respiratory processes in the anesthetized rat.

Uncoupling of upper airway motor activity from phrenic bursting by positive end-expired pressure in the rat

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