Opioid Action on Respiratory Neuron Activity of the Isolated Respiratory Network in Newborn Rats

Takeda, Satoru; Eriksson, Lars; Yamamoto, Yuji; Joensen, Hanna; Onimaru, Hiroshi; Lindahl, Sten G. E.

doi:10.1097/00000542-200109000-00029

Cited by 121 publications

(107 citation statements)

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“…RTN/pfRG provides a major excitatory drive to the central respiratory pattern generator (CPG) (Fukuda et al, 1993;Nattie and Li, 2000;Feldman et al, 2003;Onimaru and Homma, 2003), but its functional role within the respiratory network remains unclear. The phasic and often preinspiratory discharge pattern of pfRG neurons in neonate preparations supports a pacemaker neuron-based inspiratory or expiratory rhythmogenic role for pfRG (Onimaru et al, 1995;Takeda et al, 2001;Janczewski et al, 2002;Onimaru and Homma, 2003), whereas the more tonic discharge of adult RTN neurons in vivo favors a central chemoreceptor function Mulkey et al, 2004;Putnam et al, 2004).…”

Section: Introductionmentioning

confidence: 83%

“…In essence, we hypothesize that the CPG input to the chemosensitive neurons of RTN/pfRG is a simple feedback. This feedback originates from phasically active respiratory neurons and therefore produces the respiratory modulation of RTN/pfRG previously observed under various experimental conditions (Connelly et al, 1990;Nattie et al, 1993;Onimaru et al, 1995;Bodineau et al, 2000;Takeda et al, 2001;Janczewski et al, 2002;Onimaru and Homma, 2003).…”

Section: Introductionmentioning

confidence: 86%

“…Adult RTN and neonate pfRG pre-inspiratory (pre-I) neurons have a similar location (Onimaru and Homma 2003;Mulkey et al, 2004). Some pre-I pfRG neurons are also mildly activated by acidification in vitro, and, like many RTN neurons in vivo, they are relatively insensitive to morphine and their respiratory pattern is biphasic (Takeda et al, 2001;Janczewski et al, 2002;Mulkey et al, 2004). The main respiratory pattern of RTN neurons (early-I/post-I inhibition; 42% of cells with an identifiable pattern) (Fig.…”

Section: Role Of the Inhibitory Inputs From The Cpg To Rtn Neuronsmentioning

confidence: 99%

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Regulation of Ventral Surface Chemoreceptors by the Central Respiratory Pattern Generator

Guyenet

Mulkey²,

Stornetta³

et al. 2005

J. Neurosci.

163

272

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The rat retrotrapezoid nucleus (RTN) contains neurons described as central chemoreceptors in the adult and respiratory rhythmgenerating pacemakers in neonates [parafacial respiratory group (pfRG)]. Here we test the hypothesis that both RTN and pfRG neurons are intrinsically chemosensitive and tonically firing neurons whose respiratory rhythmicity is caused by a synaptic feedback from the central respiratory pattern generator (CPG). In halothane-anesthetized adults, RTN neurons were silent below 4.5% end-expiratory (e-exp) CO 2 . Their activity increased linearly (3.2 Hz/1% CO 2 ) up to 6.5% (CPG threshold) and then more slowly to peak ϳ10 Hz at 10% CO 2 . Respiratory modulation of RTN neurons was absent below CPG threshold, gradually stronger beyond, and, like pfRG neurons, typically (42%) characterized by twin periods of reduced activity near phrenic inspiration. After CPG inactivation with kynurenate (KYN), RTN neurons discharged linearly as a function of e-exp CO 2 (slope, ϩ1.7 Hz/1% CO 2 ) and arterial pH (threshold, 7.48; slope, 39 Hz/pH unit). In coronal brain slices (postnatal days 7-12), RTN chemosensitive neurons were silent at pH 7.55. Their activity increased linearly with acidification up to pH 7.2 (17 Hz/pH unit at 35°C) and was always tonic.In conclusion, consistent with their postulated central chemoreceptor role, RTN/pfRG neurons encode pH linearly and discharge tonically when disconnected from the rest of the respiratory centers in vivo (KYN treatment) and in vitro. In vivo, RTN neurons receive respiratory synchronous inhibitory inputs that may serve as feedback and impart these neurons with their characteristic respiratory modulation.

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Section: Introductionmentioning

confidence: 83%

Section: Introductionmentioning

confidence: 86%

Section: Role Of the Inhibitory Inputs From The Cpg To Rtn Neuronsmentioning

confidence: 99%

See 1 more Smart Citation

Regulation of Ventral Surface Chemoreceptors by the Central Respiratory Pattern Generator

Guyenet

Mulkey²,

Stornetta³

et al. 2005

J. Neurosci.

163

272

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“…So, why does the Dscam Ϫ/Ϫ mouse show perinatal death and why does the Dscam ϩ/Ϫ mouse can survive? The opiate surge at neonatal stage would depress the excitability of Insp neurons in the preBötC but not that of Pre-I neurons in the pFRG (Takeda et al, 2001). It is therefore hypothesized that the pFRG is an "anti-apnea" center that promotes breathing immediately after birth (Jacquin et al, 1996).…”

Section: Loss Of Pre-i Synchroneity In Dscammentioning

confidence: 99%

DSCAM Deficiency Causes Loss of Pre-Inspiratory Neuron Synchroneity and Perinatal Death

et al. 2009

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Down syndrome cell adhesion molecule (DSCAM) is a neural adhesion molecule that plays diverse roles in neural development. We disrupted the Dscam locus in mice and found that the null mutants (Dscam Ϫ/Ϫ ) died within 24 h after birth. Whole-body plethysmography showed irregular respiration and lower ventilatory response to hypercapnia in the null mutants. Furthermore, a medulla-spinal cord preparation of Dscam Ϫ/Ϫ mice showed that the C4 ventral root activity, which drives diaphragm contraction for inspiration, had an irregular rhythm with frequent apneas. Optical imaging of the preparation using voltage-sensitive dye revealed that the pre-inspiratory neurons located in the rostral ventrolateral medulla and belonging to the rhythm generator for respiration, lost their synchroneity in Dscam Ϫ/Ϫ mice. Dscam ϩ/Ϫ mice, which survived to adulthood without any overt abnormalities, also showed irregular respiration but milder than Dscam Ϫ/Ϫ mice. These results suggest that DSCAM plays a critical role in central respiratory regulation in a dosagedependent manner.

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“…The other neuronal group, the pFRG (Onimaru and Homma, 2003;Onimaru et al, 2004), contains neurons that discharge during the preinspiratory phase and that are synaptically connected to neurons of the PBC (Takeda et al, 2001;Janczewski et al, 2002;Mellen et al, 2003). Interestingly, two recent studies from Onimaru and Homma performed in rat showed (1) that neurons exhibiting a preinspiratory discharge could not be found before the developmental stage E19 and (2) using optical recordings in embryonic rat brainstem-spinal cord preparations that the pFRG might not be functional before E19 (Onimaru and Homma, 2005).…”

Section: The Hf Generator Is the Respiratory Generatormentioning

confidence: 99%

Emergence of the Pre-Bötzinger Respiratory Rhythm Generator in the Mouse Embryo

Thoby‐Brisson¹,

Trinh²,

Champagnat³

et al. 2005

J. Neurosci.

117

148

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To obtain insights into the emergence of rhythmogenic circuits supporting respiration, we monitored spontaneous activities in isolated brainstem and medullary transverse slice preparations of mouse embryos, combining electrophysiological and calcium imaging techniques. At embryonic day 15 (E15), in a restricted region ventral to the nucleus ambiguus, we observed the onset of a sustained highfrequency (HF) respiratory-like activity in addition to a preexisting low-frequency activity having a distinct initiation site, spatial extension, and susceptibility to gap junction blockers. At the time of its onset, the HF generator starts to express the neurokinin 1 receptor, is connected bilaterally, requires active AMPA/kainate glutamatergic synapses, and is modulated by substance P and the -opioid agonist D-Ala 2 -N-Me-Phe 4 -Glycol 5 -enkephalin. We conclude that a rhythm generator sharing the properties of the neonatal pre-Bötzinger complex becomes active during E15 in mice.

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Opioid Action on Respiratory Neuron Activity of the Isolated Respiratory Network in Newborn Rats

Cited by 121 publications

References 0 publications

Regulation of Ventral Surface Chemoreceptors by the Central Respiratory Pattern Generator

Regulation of Ventral Surface Chemoreceptors by the Central Respiratory Pattern Generator

DSCAM Deficiency Causes Loss of Pre-Inspiratory Neuron Synchroneity and Perinatal Death

Emergence of the Pre-Bötzinger Respiratory Rhythm Generator in the Mouse Embryo

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