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Abstract
Neuronal cell groups residing within the retrotrapezoid nucleus (RTN) and C1 area of the rostral ventrolateral medulla oblongata contribute to the maintenance of resting respiratory activity and arterial blood pressure, and play an important role in the development of cardiorespiratory responses to metabolic challenges (such as hypercapnia and hypoxia). In rats, acute silencing of neurons within the parafacial region which includes the RTN and the rostral aspect of the C1 circuit (pFRTN/C1), transduced to express HM4D (Gi-coupled) receptors, was found to dramatically reduce exercise capacity (by 60%), determined by an intensity controlled treadmill running test. In a model of simulated exercise (electrical stimulation of the sciatic or femoral nerve in urethane anaesthetised spontaneously breathing rats) silencing of the pFRTN/C1 neurons had no effect on cardiovascular changes, but significantly reduced the respiratory response during steady state exercise. These results identify a neuronal cell group in the lower brainstem which is critically important for the development of the respiratory response to exercise and, determines exercise capacity.
Highlights
In the parafacial region of the rostral ventrolateral medulla oblongata a distinct group of neurons which reside within the retrotrapezoid nucleus (RTN) control breathing by integrating chemosensory information received from other CNS structures[16,17,18,19], local astrocytes[20,21,22], and the peripheral chemoreceptors[16,23,24]
The majority of transduced HM4D (Gi-DREADD) receptor (HM4DR)-expressing neurons (119 ± 8 per side), were considered to be parafacial RTN neurons based on their anatomical location in relation to the facial nucleus[28,34]
We tested the hypothesis that functional neuronal groups which reside in the parafacial region of the brainstem, including RTN and C1 cell populations, orchestrate cardiorespiratory responses during exercise
Summary
In the parafacial region of the rostral ventrolateral medulla oblongata a distinct group of neurons which reside within the retrotrapezoid nucleus (RTN) control breathing by integrating chemosensory information received from other CNS structures[16,17,18,19], local astrocytes[20,21,22], and the peripheral chemoreceptors[16,23,24]. There is evidence that the RTN neurons are critically important for the recruitment of active expiratory activity[28,29,30], and that these neurons are activated during exercise[31] Another notable brainstem neuronal population, which resides in close proximity to the RTN, is the C1 catecholaminergic cell group which contributes to the generation of central sympathetic drive and is critically important for cardiovascular control in conditions of increased metabolic demand[27,32]. We hypothesised that these two important neuronal populations orchestrate the cardiovascular (C1 neurons) and respiratory (RTN neurons) responses to exercise and, by doing so, determine exercise capacity. We determined the effect of inhibiting this region on exercise capacity (Fig. 1B), and cardiovascular and respiratory responses to simulated exercise (electrical sciatic or femoral nerve stimulation in urethane anaesthetised spontaneously breathing rats; Fig. 1C)
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