Connections between retrotrapezoid nucleus and nucleus tractus solitarii in cat

Bodineau, Laurence; Frugière, Alain; Marlot, D.; Wallois, Fabrice

doi:10.1016/s0304-3940(00)00770-9

Cited by 23 publications

(23 citation statements)

References 7 publications

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“…In any event, the present results are consistent with prior electrophysiological evidence that commNTS cells with carotid chemoreceptor input innervate the rostral ventrolateral medulla in rats and the RTN region of cats (Koshiya & Guyenet, 1996;Bodineau et al 2000a).…”

Section: Figure 12 Possible Role Of Rtn In Chemosensory Integrationsupporting

confidence: 92%

Peripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO₂‐sensitive neurons in rats

Takakura

Moreira

Colombari

et al. 2006

The Journal of Physiology

292

329

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The rat retrotrapezoid nucleus (RTN) contains pH-sensitive neurons that are putative central chemoreceptors. Here, we examined whether these neurons respond to peripheral chemoreceptor stimulation and whether the input is direct from the solitary tract nucleus (NTS) or indirect via the respiratory network. A dense neuronal projection from commissural NTS (commNTS) to RTN was revealed using the anterograde tracer biotinylated dextran amine (BDA). Within RTN, 51% of BDA-labelled axonal varicosities contained detectable levels of vesicular glutamate transporter-2 (VGLUT2) but only 5% contained glutamic acid decarboxylase-67 (GAD67). Awake rats were exposed to hypoxia (n = 6) or normoxia (n = 5) 1 week after injection of the retrograde tracer cholera toxin B (CTB) into RTN. Hypoxia-activated neurons were identified by the presence of Fos-immunoreactive nuclei. CommNTS neurons immunoreactive for both Fos and CTB were found only in hypoxia-treated rats. VGLUT2 mRNA was detected in 92 ± 13% of these neurons whereas only 12 ± 9% contained GAD67 mRNA. In urethane-chloralose-anaesthetized rats, bilateral inhibition of the RTN with muscimol eliminated the phrenic nerve discharge (PND) at rest, during hyperoxic hypercapnia (10% CO 2 ), and during peripheral chemoreceptor stimulation (hypoxia and/or I.V. sodium cyanide, NaCN). RTN CO 2 -activated neurons were recorded extracellularly in anaesthetized intact or vagotomized rats. These neurons were strongly activated by hypoxia (10-15% O 2 ; 30 s) or by NaCN. Hypoxia and NaCN were ineffective in rats with carotid chemoreceptor denervation. Bilateral injection of muscimol into the ventral respiratory column 1.5 mm caudal to RTN eliminated PND and the respiratory modulation of RTN neurons. Muscimol did not change the threshold and sensitivity of RTN neurons to hyperoxic hypercapnia nor their activation by peripheral chemoreceptor stimulation. In conclusion, RTN neurons respond to brain P CO 2 presumably via their intrinsic chemosensitivity and to carotid chemoreceptor activation via a direct glutamatergic pathway from commNTS that bypasses the respiratory network. RTN neurons probably contribute a portion of the chemical drive to breathe. The chemical drive to breathe relies on central chemoreceptors that detect brain extracellular fluid P CO 2 via pH, and on carotid body chemoreceptors that respond to arterial P CO 2 in a P O 2 -and glucose-dependent manner (Scheid et al.

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Section: Figure 12 Possible Role Of Rtn In Chemosensory Integrationsupporting

confidence: 92%

Peripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO₂‐sensitive neurons in rats

Takakura

Moreira

Colombari

et al. 2006

The Journal of Physiology

292

329

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“…Alternatively, the interaction could take place in higher regions of the central nervous system, which would agree with the view of Ishida et al (20). Sites that influence respiratory control that are known to receive sensory input and/or respond to states of arousal include medullary reticular neurons (6,11,45), the retrotrapezoid nucleus (7,12,31), the nucleus reticularis gigantocellularis (37), and the nucleus tractus solitarius (35,36,39).…”

Section: Discussionsupporting

confidence: 78%

Respiratory response to passive limb movement is suppressed by a cognitive task

Bell

Duffin²

2004

Journal of Applied Physiology

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Bell, Harold J., and James Duffin. Respiratory response to passive limb movement is suppressed by a cognitive task. J Appl Physiol 97: 2112-2120, 2004. First published July 23, 2004 doi: 10.1152/japplphysiol.00302.2004.-Feedback from muscles stimulates ventilation at the onset of passive movement. We hypothesized that central neural activity via a cognitive task source would interact with afferent feedback, and we tested this hypothesis by examining the fast changes in ventilation at the transition from rest to passive leg movement, under two conditions: 1) no task and 2) solving a computer-based puzzle. Resting breathing was greater in condition 2 than in condition 1, evidenced by an increase in mean Ϯ SE breathing frequency (18.2 Ϯ 1.1 vs. 15.0 Ϯ 1.2 breaths/min, P ϭ 0.004) and ventilation (10.93 Ϯ 1.16 vs. 9.11 Ϯ 1.17 l/min, P Ͻ 0.001). In condition 1, the onset of passive movement produced a fast increase in mean Ϯ SE breathing frequency (change of 2.9 Ϯ 0.4 breaths/min, P Ͻ 0.001), tidal volume (change of 233 Ϯ 95 ml, P Ͻ 0.001), and ventilation (change of 6.00 Ϯ 1.76 l/min, P Ͻ 0.001). However, in condition 2, the onset of passive movement only produced a fast increase in mean Ϯ SE breathing frequency (change of 1.3 Ϯ 0.4 breaths/min, P ϭ 0.045), significantly smaller than in condition 1 (P ϭ 0.007). These findings provide evidence for an interaction between central neural cognitive activity and the afferent feedback mechanism, and we conclude that the performance of a cognitive task suppresses the respiratory response to passive movement. exercise hyperpnea; wakefulness drive; afferent feedback AT THE ONSET OF EXERCISE, ventilation (V E) increases immediately (25), and the rapid onset of this drive to breathe has led to it being assigned a neural origin, since it is too fast for a humoral source (15,26). This "exercise drive to breathing" is hypothesized to result from two sources: one is "peripheral neurogenic drive," whereby afferent feedback from the exercising limbs leads to increased respiration (21); the other is "central command," whereby motor commands to the limbs initiate a parallel activation of respiration (17,49).In the integrated system, both of these mechanisms are initiated simultaneously; therefore, any interaction between them could affect their respective contributions toward the control of breathing. Indeed, animal model studies have provided evidence of interactions between central motor commands and afferent feedback (2, 13, 37). Such findings support the idea that, at the onset of exercise, neural drives to breathe via distinct mechanisms are incorporated to provide the drive to breathe that is observed in the integrated system.The onset of exercise also involves an increase in central neural activity via cortical brain activity (23, 32) that is not solely related to the motor outflow to the muscles itself. For example, during imagined exercise where both central motor command and afferent feedback mechanisms are absent, significant increases in cortical activity occur and this act...

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“…Inputs from peripheral carotid chemoreceptors to the chemosensitive RTN neurons provide a mechanism for the integration of peripheral and central chemoreflexes (Mulkey et al, 2004;Takakura et al, 2006). Stimulation of ventrolateral NTS [an area that contains cells retrogradely labeled from RTN (current study) and bulbospinal respiratory neurons] also activates RTN neurons (Bodineau et al, 2000b). Finally, commissural NTS projects to many of the same regions in which we found RTN projections (i.e., parabrachial and Kolliker-Fuse nuclei, region of the A5 noradrenergic cell group, and VRC; Otake et al, 1992), suggesting a convergence of information from peripheral and central chemoreceptors on central autonomic regulatory regions and specifically on pontomedullary areas involved in cardiorespiratory homeostasis.…”

Section: Functional Significance Of Connections Of Rtnmentioning

confidence: 82%

Afferent and efferent connections of the rat retrotrapezoid nucleus

2006

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The rat retrotrapezoid nucleus (RTN) contains candidate central chemoreceptors that have extensive dendrites within the marginal layer (ML). This study describes the axonal projections of RTN neurons and their probable synaptic inputs. The ML showed a dense plexus of nerve terminals immunoreactive (ir) for markers of glutamatergic (vesicular glutamate transporters VGLUT1-3), gamma-aminobutyric acid (GABA)-ergic, adrenergic, serotonergic, cholinergic, and peptidergic transmission. The density of VGLUT3-ir terminals tracked the location of RTN chemoreceptors. The efferent and afferent projections of RTN were studied by placing small iontophoretic injections of anterograde (biotinylated dextran amine; BDA) and retrograde (cholera toxin B) tracers where RTN chemoreceptors have been previously recorded. BDA did not label the nearby C1 cells. BDA-ir varicosities were found in the solitary tract nucleus (NTS), all ventral respiratory column (VRC) subdivisions, A5 noradrenergic area, parabrachial complex, and spinal cord. In each target region, a large percentage of the BDA-ir varicosities was VGLUT2-ir (41-83%). Putative afferent input to RTN originated from spinal cord, caudal NTS, area postrema, VRC, dorsolateral pons, raphe nuclei, lateral hypothalamus, central amygdala, and insular cortex. The results suggest that 1) whether or not the ML is specialized for CO(2) sensing, its complex neuropil likely regulates the activity of RTN chemosensitive neurons; 2) the catecholaminergic, cholinergic, and serotonergic innervation of RTN represents a possible substrate for the known state-dependent control of RTN chemoreceptors; 3) VGLUT3-ir terminals are a probable marker of RTN; and 4) the chemosensitive neurons of RTN may provide a chemical drive to multiple respiratory outflows, insofar as RTN innervates the entire VRC.

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Connections between retrotrapezoid nucleus and nucleus tractus solitarii in cat

Cited by 23 publications

References 7 publications

Peripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO₂‐sensitive neurons in rats

Peripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO₂‐sensitive neurons in rats

Respiratory response to passive limb movement is suppressed by a cognitive task

Afferent and efferent connections of the rat retrotrapezoid nucleus

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Connections between retrotrapezoid nucleus and nucleus tractus solitarii in cat

Cited by 23 publications

References 7 publications

Peripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO2‐sensitive neurons in rats

Peripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO2‐sensitive neurons in rats

Respiratory response to passive limb movement is suppressed by a cognitive task

Afferent and efferent connections of the rat retrotrapezoid nucleus

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Peripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO₂‐sensitive neurons in rats

Peripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO₂‐sensitive neurons in rats