Non‐chemosensitive parafacial neurons simultaneously regulate active expiration and airway patency under hypercapnia in rats

Britto, Alan A. de; Moraes, Davi J. A.

doi:10.1113/jp273335

Cited by 51 publications

(120 citation statements)

References 34 publications

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“…Expiratory abdominal muscle recruitment varies according to behavioural states. Active expiration occurs during periods of high metabolic demand, and this phenomenon has been shown to be driven by the parafacial respiratory group in the medulla (de Britto & Moraes, 2017;Huckstepp, Cardoza, Henderson, & Feldman, 2015;Janczewski & Feldman, 2006;Pagliardini et al, 2011). Besides wakefulness, active expiration has previously been reported to occur during both NREM and REM sleep in eupnoeic conditions (rats breathing room air; Andrews & Pagliardini, 2015;Pisanski & Pagliardini, 2018;Sherrey et al, 1988).…”

Section: Expiratory Activity During the Sleep-wake Cycle After Cihmentioning

confidence: 99%

Cardiovascular and respiratory profiles during the sleep–wake cycle of rats previously submitted to chronic intermittent hypoxia

Bazilio

Bonagamba

Moraes

et al. 2019

Experimental Physiology

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New Findings What is the central question of this study?Chronic intermittent hypoxia (CIH) causes increased arterial pressure (AP), sympathetic overactivity and changes in expiratory modulation of sympathetic activity. However, changes in the short‐term sleep–wake cycle pattern after CIH and their potential impact on cardiorespiratory parameters have not been reported previously. What is the main finding and its importance?Exposure to CIH for 10 days elevates AP in wakefulness and sleep but does not cause major changes in short‐term sleep–wake cycle pattern. A higher incidence of muscular expiratory activity was observed in rats exposed to CIH only during wakefulness, indicating that active expiration is not required for the increase in AP in rats submitted to CIH. Abstract Chronic intermittent hypoxia (CIH) increases arterial pressure (AP) and changes sympathetic–respiratory coupling. However, the alterations in the sleep–wake cycle after CIH and their potential impact on cardiorespiratory parameters remain unknown. Here, we evaluated whether CIH‐exposed rats present changes in their short‐term sleep–wake cycle pattern and in cardiorespiratory parameters. Male Wistar rats (∼250 g) were divided into CIH and control groups. The CIH rats were exposed to 8 h day−1 of cycles of normoxia (fraction of inspired O2 = 0.208, 5 min) followed by hypoxia (fraction of inspired O2 = 0.06, 30–40 s) for 10 days. One day after CIH, electrocorticographic activity, cervical EMG, AP and heart rate were recorded for 3 h. Plethysmographic recordings were collected for 2 h. A subgroup of control and CIH rats also had the diaphragm and oblique abdominal muscle activities recorded. Chronic intermittent hypoxia did not alter the time for sleep onset, total time awake, durations of rapid eye movement (REM) and non‐REM (NREM) sleep and number of REM episodes in the 3 h recordings. However, a significant increase in the duration of REM episodes was observed. The AP and heart rate were increased in all phases of the cycle in rats exposed to CIH. Respiratory frequency and ventilation were similar between groups in all phases, but tidal volume was increased during NREM and REM sleep in rats exposed to CIH. An increase in the incidence of active expiration during wakefulness was observed in rats exposed to CIH. The data show that CIH‐related hypertension is not caused by changes in the sleep–wake cycle and suggest that active expiration is not required for the increase in AP in freely moving rats exposed to CIH.

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Section: Expiratory Activity During the Sleep-wake Cycle After Cihmentioning

confidence: 99%

Cardiovascular and respiratory profiles during the sleep–wake cycle of rats previously submitted to chronic intermittent hypoxia

Bazilio

Bonagamba

Moraes

et al. 2019

Experimental Physiology

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“…Thus, both gain and loss of function experiments show that RTN neurons stimulate multiple aspects of breathing, including active expiration. Whether RTN neurons and the proposed parafacial 'oscillator for active expiration' are one and the same, overlapping or entirely separate neuronal populations remains to be determined (Janczewski & Feldman, 2006;Pagliardini et al 2011;Huckstepp et al 2015Huckstepp et al , 2016de Britto & Moraes, 2017).…”

Section: Rtn Neurons Drive Multiple Aspects Of Breathing Including Amentioning

confidence: 99%

Interdependent feedback regulation of breathing by the carotid bodies and the retrotrapezoid nucleus

Guyenet

Bayliss

Kanbar

et al. 2017

The Journal of Physiology

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The retrotrapezoid nucleus (RTN) regulates breathing in a CO - and state-dependent manner. RTN neurons are glutamatergic and innervate principally the respiratory pattern generator; they regulate multiple aspects of breathing, including active expiration, and maintain breathing automaticity during non-REM sleep. RTN neurons encode arterial /pH via cell-autonomous and paracrine mechanisms, and via input from other CO -responsive neurons. In short, RTN neurons are a pivotal structure for breathing automaticity and arterial homeostasis. The carotid bodies stimulate the respiratory pattern generator directly and indirectly by activating RTN via a neuronal projection originating within the solitary tract nucleus. The indirect pathway operates under normo- or hypercapnic conditions; under respiratory alkalosis (e.g. hypoxia) RTN neurons are silent and the excitatory input from the carotid bodies is suppressed. Also, silencing RTN neurons optogenetically quickly triggers a compensatory increase in carotid body activity. Thus, in conscious mammals, breathing is subject to a dual and interdependent feedback regulation by chemoreceptors. Depending on the circumstance, the activity of the carotid bodies and that of RTN vary in the same or the opposite directions, producing additive or countervailing effects on breathing. These interactions are mediated either via changes in blood gases or by brainstem neuronal connections, but their ultimate effect is invariably to minimize arterial fluctuations. We discuss the potential relevance of this dual chemoreceptor feedback to cardiorespiratory abnormalities present in diseases in which the carotid bodies are hyperactive at rest, e.g. essential hypertension, obstructive sleep apnoea and heart failure.

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“…Evidence of hypercapnia‐induced expiratory abdominal activity in rats extends from in situ preparations (Abdala et al . ; de Britto & Moraes, ; Jenkin et al . ) to in vivo anaesthetized animals (Iizuka & Fregosi, ; Lemes & Zoccal, ), but whether active expiration occurs in unanaesthetized animals under hypercapnic conditions in a state‐dependent manner, i.e.…”

Section: Introductionmentioning

confidence: 99%

“…Interestingly, however, under eupnoeic conditions, where active expiration is absent normally, abdominal activity emerges in the REM-like sleep state in urethane-anaesthetized rats as well as in REM sleep, providing stability to breathing (Pagliardini et al 2012;Andrews & Pagliardini, 2015). Evidence of hypercapnia-induced expiratory abdominal activity in rats extends from in situ preparations (Abdala et al 2009;de Britto & Moraes, 2016;Jenkin et al 2017) to in vivo anaesthetized animals (Iizuka & Fregosi, 2007;Lemes & Zoccal, 2014), but whether active expiration occurs in unanaesthetized animals under hypercapnic conditions in a state-dependent manner, i.e. differently in sleep and wakefulness, remains to be seen.…”

Section: Introductionmentioning

confidence: 99%

Hypercapnia‐induced active expiration increases in sleep and enhances ventilation in unanaesthetized rats

Leirão

Silva

Gargaglioni

et al. 2017

The Journal of Physiology

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Expiration is passive at rest but becomes active through recruitment of abdominal muscles under increased respiratory drive. Hypercapnia-induced active expiration has not been well explored in unanaesthetized rats. We hypothesized that (i) CO -evoked active expiration is recruited in a state-dependent manner, i.e. differently in sleep or wakefulness, and (ii) recruitment of active expiration enhances ventilation, hence having an important functional role in meeting metabolic demand. To test these hypotheses, Wistar rats (280-330 g) were implanted with electrodes for EEG and electromyography EMG of the neck, diaphragm (DIA) and abdominal (ABD) muscles. Active expiratory events were considered as rhythmic ABD activity interposed to DIA . Animals were exposed to room air followed by hypercapnia (7% CO ) with EEG, EMG and ventilation ( ) recorded throughout the experimental protocol. No active expiration was observed during room air exposure. During hypercapnia, CO -evoked active expiration was predominantly recruited during non-rapid eye movement sleep. Its increased occurrence during sleep was evidenced by the decreased DIA-to-ADB ratio (1:1 ratio means that each DIA event is followed by an ABD event, indicating a high occurrence of ABD activity). Moreover, was also enhanced (P< 0.05) in periods with active expiration. had a positive correlation (P< 0.05) with the peak amplitude of ABD activity. The data demonstrate strongly that hypercapnia-induced active expiration increases during sleep and provides an important functional role to support in conditions of increased respiratory demand.

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Non‐chemosensitive parafacial neurons simultaneously regulate active expiration and airway patency under hypercapnia in rats

Cited by 51 publications

References 34 publications

Cardiovascular and respiratory profiles during the sleep–wake cycle of rats previously submitted to chronic intermittent hypoxia

Cardiovascular and respiratory profiles during the sleep–wake cycle of rats previously submitted to chronic intermittent hypoxia

Interdependent feedback regulation of breathing by the carotid bodies and the retrotrapezoid nucleus

Hypercapnia‐induced active expiration increases in sleep and enhances ventilation in unanaesthetized rats

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