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Articles de revues sur le sujet « Respiratory rhythm generation »

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Auteur : Grafiati
Publié le 10 mars 2023

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1

Anderson, Tatiana M., et Jan-Marino Ramirez. « Respiratory rhythm generation : triple oscillator hypothesis ». F1000Research 6 (14 février 2017) : 139. http://dx.doi.org/10.12688/f1000research.10193.1.

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Breathing is vital for survival but also interesting from the perspective of rhythm generation. This rhythmic behavior is generated within the brainstem and is thought to emerge through the interaction between independent oscillatory neuronal networks. In mammals, breathing is composed of three phases – inspiration, post-inspiration, and active expiration – and this article discusses the concept that each phase is generated by anatomically distinct rhythm-generating networks: the preBötzinger complex (preBötC), the post-inspiratory complex (PiCo), and the lateral parafacial nucleus (pFL), respectively. The preBötC was first discovered 25 years ago and was shown to be both necessary and sufficient for the generation of inspiration. More recently, networks have been described that are responsible for post-inspiration and active expiration. Here, we attempt to collate the current knowledge and hypotheses regarding how respiratory rhythms are generated, the role that inhibition plays, and the interactions between the medullary networks. Our considerations may have implications for rhythm generation in general.
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Duffin, James, et Seward Hung. « Respiratory rhythm generation ». Canadian Anaesthetists’ Society Journal 32, no 2 (mars 1985) : 124–37. http://dx.doi.org/10.1007/bf03010035.

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Richter, Diethelm W., et Jeffrey C. Smith. « Respiratory Rhythm Generation In Vivo ». Physiology 29, no 1 (janvier 2014) : 58–71. http://dx.doi.org/10.1152/physiol.00035.2013.

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The cellular and circuit mechanisms generating the rhythm of breathing in mammals have been under intense investigation for decades. Here, we try to integrate the key discoveries into an updated description of the basic neural processes generating respiratory rhythm under in vivo conditions.
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Greer, John J. « Development of respiratory rhythm generation ». Journal of Applied Physiology 104, no 4 (avril 2008) : 1211–12. http://dx.doi.org/10.1152/japplphysiol.00043.2008.

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Richter, Diethelm W., Klaus Ballanyi et Stephen Schwarzacher. « Mechanisms of respiratory rhythm generation ». Current Biology 2, no 12 (décembre 1992) : 628. http://dx.doi.org/10.1016/0960-9822(92)90094-q.

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Richter, Diethelm W., Klaus Ballanyi et Stephan Schwarzacher. « Mechanisms of respiratory rhythm generation ». Current Opinion in Neurobiology 2, no 6 (décembre 1992) : 788–93. http://dx.doi.org/10.1016/0959-4388(92)90135-8.

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Duffin, James. « A model of respiratory rhythm generation ». NeuroReport 2, no 10 (octobre 1991) : 623–26. http://dx.doi.org/10.1097/00001756-199110000-00018.

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Fortin, Gilles, Arthur S. Foutz et Jean Champagnat. « Respiratory rhythm generation in chick hindbrain ». NeuroReport 5, no 9 (mai 1994) : 1137–40. http://dx.doi.org/10.1097/00001756-199405000-00029.

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Haji, Akira, Mari Okazaki et Ryuji Takeda. « Neurotransmission mechanisms in respiratory rhythm generation ». Japanese Journal of Pharmacology 79 (1999) : 15. http://dx.doi.org/10.1016/s0021-5198(19)34088-0.

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Smith, J. C., A. P. L. Abdala, H. Koizumi, I. A. Rybak et J. F. R. Paton. « Spatial and Functional Architecture of the Mammalian Brain Stem Respiratory Network : A Hierarchy of Three Oscillatory Mechanisms ». Journal of Neurophysiology 98, no 6 (décembre 2007) : 3370–87. http://dx.doi.org/10.1152/jn.00985.2007.

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Mammalian central pattern generators (CPGs) producing rhythmic movements exhibit extremely robust and flexible behavior. Network architectures that enable these features are not well understood. Here we studied organization of the brain stem respiratory CPG. By sequential rostral to caudal transections through the pontine-medullary respiratory network within an in situ perfused rat brain stem–spinal cord preparation, we showed that network dynamics reorganized and new rhythmogenic mechanisms emerged. The normal three-phase respiratory rhythm transformed to a two-phase and then to a one-phase rhythm as the network was reduced. Expression of the three-phase rhythm required the presence of the pons, generation of the two-phase rhythm depended on the integrity of Bötzinger and pre-Bötzinger complexes and interactions between them, and the one-phase rhythm was generated within the pre-Bötzinger complex. Transformation from the three-phase to a two-phase pattern also occurred in intact preparations when chloride-mediated synaptic inhibition was reduced. In contrast to the three-phase and two-phase rhythms, the one-phase rhythm was abolished by blockade of persistent sodium current ( INaP). A model of the respiratory network was developed to reproduce and explain these observations. The model incorporated interacting populations of respiratory neurons within spatially organized brain stem compartments. Our simulations reproduced the respiratory patterns recorded from intact and sequentially reduced preparations. Our results suggest that the three-phase and two-phase rhythms involve inhibitory network interactions, whereas the one-phase rhythm depends on INaP. We conclude that the respiratory network has rhythmogenic capabilities at multiple levels of network organization, allowing expression of motor patterns specific for various physiological and pathophysiological respiratory behaviors.
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Ramirez, Jan-Marino, et Diethelm W. Richter. « The neuronal mechanisms of respiratory rhythm generation ». Current Opinion in Neurobiology 6, no 6 (décembre 1996) : 817–25. http://dx.doi.org/10.1016/s0959-4388(96)80033-x.

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12

McCrimmon, Donald R., Jan-Marino Ramirez, Simon Alford et Edward J. Zuperku. « Unraveling the mechanism for respiratory rhythm generation ». BioEssays 22, no 1 (24 janvier 2000) : 6–9. http://dx.doi.org/10.1002/(sici)1521-1878(200001)22:1<6 ::aid-bies3>3.0.co;2-q.

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Lorea-Hernández, Jonathan-Julio, Teresa Morales, Ana-Julia Rivera-Angulo, David Alcantara-Gonzalez et Fernando Peña-Ortega. « Microglia modulate respiratory rhythm generation and autoresuscitation ». Glia 64, no 4 (17 décembre 2015) : 603–19. http://dx.doi.org/10.1002/glia.22951.

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Harris, Kameron Decker, Tatiana Dashevskiy, Joshua Mendoza, Alfredo J. Garcia, Jan-Marino Ramirez et Eric Shea-Brown. « Different roles for inhibition in the rhythm-generating respiratory network ». Journal of Neurophysiology 118, no 4 (1 octobre 2017) : 2070–88. http://dx.doi.org/10.1152/jn.00174.2017.

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Unraveling the interplay of excitation and inhibition within rhythm-generating networks remains a fundamental issue in neuroscience. We use a biophysical model to investigate the different roles of local and long-range inhibition in the respiratory network, a key component of which is the pre-Bötzinger complex inspiratory microcircuit. Increasing inhibition within the microcircuit results in a limited number of out-of-phase neurons before rhythmicity and synchrony degenerate. Thus unstructured local inhibition is destabilizing and cannot support the generation of more than one rhythm. A two-phase rhythm requires restructuring the network into two microcircuits coupled by long-range inhibition in the manner of a half-center. In this context, inhibition leads to greater stability of the two out-of-phase rhythms. We support our computational results with in vitro recordings from mouse pre-Bötzinger complex. Partial excitation block leads to increased rhythmic variability, but this recovers after blockade of inhibition. Our results support the idea that local inhibition in the pre-Bötzinger complex is present to allow for descending control of synchrony or robustness to adverse conditions like hypoxia. We conclude that the balance of inhibition and excitation determines the stability of rhythmogenesis, but with opposite roles within and between areas. These different inhibitory roles may apply to a variety of rhythmic behaviors that emerge in widespread pattern-generating circuits of the nervous system. NEW & NOTEWORTHY The roles of inhibition within the pre-Bötzinger complex (preBötC) are a matter of debate. Using a combination of modeling and experiment, we demonstrate that inhibition affects synchrony, period variability, and overall frequency of the preBötC and coupled rhythmogenic networks. This work expands our understanding of ubiquitous motor and cognitive oscillatory networks.
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Ramirez, Jan-Marino, Tatiana Dashevskiy, Ibis Agosto Marlin et Nathan Baertsch. « Microcircuits in respiratory rhythm generation : commonalities with other rhythm generating networks and evolutionary perspectives ». Current Opinion in Neurobiology 41 (décembre 2016) : 53–61. http://dx.doi.org/10.1016/j.conb.2016.08.003.

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Gajda, B. M., A. Y. Fong et W. K. Milsom. « Species differences in respiratory rhythm generation in rodents ». American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no 4 (avril 2010) : R887—R898. http://dx.doi.org/10.1152/ajpregu.00339.2009.

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We examined the role of riluzole (RIL)- and flufenamic acid (FFA)-sensitive mechanisms in respiratory rhythmogenesis in rats and hamsters using the in situ arterially perfused preparation. Based on the hypothesis that respiratory networks in animals capable of autoresuscitation would have a greater prevalence of membrane mechanisms that promote endogenous bursting, we predicted that older (weaned) hamsters (a hibernating species) would be more sensitive to the blockade of RIL- and FFA-sensitive mechanisms than age-matched rats and that younger (preweaned) rats would behave more like hamsters. Consistent with this, we found that respiratory motor output in weaned hamsters [>21 days postnatal (P21)] was highly sensitive to RIL (0.2–20 μM), while in young rats (P12–14) it was less so (only affected at higher concentrations of RIL), and weaned rats were not affected at all. On the other hand, respiratory motor output was equally reduced by FFA (0.25–25 μM) in both young and weaned rats but was unaffected in weaned hamsters. Coapplication of RIL and FFA (RIL + FFA) produced greater inhibition of respiration in both young and weaned rats compared with either drug alone. In contrast, in weaned hamsters, FFA coapplication offset the inhibitory effect of RIL alone. Increasing respiratory drive with hypercapnia/acidosis ameliorated the respiratory inhibition produced by RIL + FFA in weaned rats but had no effect in young rats. Data from the present study indicate that respiratory rhythmogenesis in young rats is more dependent on excitatory RIL-sensitive and FFA-sensitive mechanisms than older rats and that fundamental differences exist in the respiratory rhythmogenic mechanisms between rats and hamsters.
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17

Del Negro, Christopher A., et John A. Hayes. « A ‘group pacemaker’ mechanism for respiratory rhythm generation ». Journal of Physiology 586, no 9 (1 mai 2008) : 2245–46. http://dx.doi.org/10.1113/jphysiol.2008.153627.

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18

Richter, Diethelm W., Sergej L. Mironov, Dietrich Büsselberg, Peter M. Lalley, Anne M. Bischoff et Bernd Wilken. « Respiratory Rhythm Generation : Plasticity of a Neuronal Network ». Neuroscientist 6, no 3 (juin 2000) : 181–98. http://dx.doi.org/10.1177/107385840000600309.

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19

Hedrick, Michael S. « Development of respiratory rhythm generation in ectothermic vertebrates ». Respiratory Physiology & ; Neurobiology 149, no 1-3 (novembre 2005) : 29–41. http://dx.doi.org/10.1016/j.resp.2005.03.019.

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Rubin, Jonathan E., et Jeffrey C. Smith. « Robustness of respiratory rhythm generation across dynamic regimes ». PLOS Computational Biology 15, no 7 (30 juillet 2019) : e1006860. http://dx.doi.org/10.1371/journal.pcbi.1006860.

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Rybak, L. A., et J. S. Schwaber. « Computational Model of Network-Based Respiratory Rhythm Generation ». IFAC Proceedings Volumes 27, no 1 (mars 1994) : 575–76. http://dx.doi.org/10.1016/s1474-6670(17)46343-9.

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Onimaru, Hiroshi, Kayo Tsuzawa, Yoshimi Nakazono et Wiktor A. Janczewski. « Midline section of the medulla abolishes inspiratory activity and desynchronizes pre-inspiratory neuron rhythm on both sides of the medulla in newborn rats ». Journal of Neurophysiology 113, no 7 (avril 2015) : 2871–78. http://dx.doi.org/10.1152/jn.00554.2014.

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Each half of the medulla contains respiratory neurons that constitute two generators that control respiratory rhythm. One generator consists of the inspiratory neurons in the pre-Bötzinger complex (preBötC); the other, the pre-inspiratory (Pre-I) neurons in the parafacial respiratory group (pFRG), rostral to the preBötC. We investigated the contribution of the commissural fibers, connecting the respiratory rhythm generators located on the opposite side of the medulla to the generation of respiratory activity in brain stem-spinal cord preparation from 0- to 1-day-old rats. Pre-I neuron activity and the facial nerve and/or first lumbar (L1) root activity were recorded as indicators of the pFRG-driven rhythm. Fourth cervical ventral root (C4) root and/or hypoglossal (XII) nerve activity were recorded as indicators of preBötC-driven inspiratory activity. We found that a midline section that interrupted crossed fibers rostral to the obex irreversibly eliminated C4 and XII root activity, whereas the Pre-I neurons, facial nerve, and L1 roots remained rhythmically active. The facial and contralateral L1 nerve activities were synchronous, whereas right and left facial (and right and left L1) nerves lost synchrony. Optical recordings demonstrated that pFRG-driven burst activity was preserved after a midline section, whereas the preBötC neurons were no longer rhythmic. We conclude that in newborn rats, crossed excitatory interactions (via commissural fibers) are necessary for the generation of inspiratory bursts but not for the generation of rhythmic Pre-I neuron activity.
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Guerrier, Claire, John A. Hayes, Gilles Fortin et David Holcman. « Robust network oscillations during mammalian respiratory rhythm generation driven by synaptic dynamics ». Proceedings of the National Academy of Sciences 112, no 31 (20 juillet 2015) : 9728–33. http://dx.doi.org/10.1073/pnas.1421997112.

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How might synaptic dynamics generate synchronous oscillations in neuronal networks? We address this question in the preBötzinger complex (preBötC), a brainstem neural network that paces robust, yet labile, inspiration in mammals. The preBötC is composed of a few hundred neurons that alternate bursting activity with silent periods, but the mechanism underlying this vital rhythm remains elusive. Using a computational approach to model a randomly connected neuronal network that relies on short-term synaptic facilitation (SF) and depression (SD), we show that synaptic fluctuations can initiate population activities through recurrent excitation. We also show that a two-step SD process allows activity in the network to synchronize (bursts) and generate a population refractory period (silence). The model was validated against an array of experimental conditions, which recapitulate several processes the preBötC may experience. Consistent with the modeling assumptions, we reveal, by electrophysiological recordings, that SF/SD can occur at preBötC synapses on timescales that influence rhythmic population activity. We conclude that nondeterministic neuronal spiking and dynamic synaptic strengths in a randomly connected network are sufficient to give rise to regular respiratory-like rhythmic network activity and lability, which may play an important role in generating the rhythm for breathing and other coordinated motor activities in mammals.
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Ramirez, J. M., P. Telgkamp, F. P. Elsen, U. J. A. Quellmalz et D. W. Richter. « Respiratory rhythm generation in mammals : synaptic and membrane properties ». Respiration Physiology 110, no 2-3 (novembre 1997) : 71–85. http://dx.doi.org/10.1016/s0034-5687(97)00074-1.

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Bongianni, Fulvia, Donatella Mutolo, Elenia Cinelli et Tito Pantaleo. « Neural mechanisms underlying respiratory rhythm generation in the lamprey ». Respiratory Physiology & ; Neurobiology 224 (avril 2016) : 17–26. http://dx.doi.org/10.1016/j.resp.2014.09.003.

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Zavala-Tecuapetla, C., M. A. Aguileta, J. J. Lopez-Guerrero, M. C. González-Marín et F. Peña. « Calcium-activated potassium currents differentially modulate respiratory rhythm generation ». European Journal of Neuroscience 27, no 11 (juin 2008) : 2871–84. http://dx.doi.org/10.1111/j.1460-9568.2008.06214.x.

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Rybak, I. A., J. F. R. Paton, R. F. Rogers et W. M. St.-John. « Generation of the respiratory rhythm : state-dependency and switching ». Neurocomputing 44-46 (juin 2002) : 605–14. http://dx.doi.org/10.1016/s0925-2312(02)00447-2.

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Champagnat, Jean, et Gilles Fortin. « Primordial respiratory-like rhythm generation in the vertebrate embryo ». Trends in Neurosciences 20, no 3 (mars 1997) : 119–24. http://dx.doi.org/10.1016/s0166-2236(96)10078-3.

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Es'kov, V. M., et O. E. Filatova. « Respiratory rhythm generation in rats : The importance of inhibition ». Neurophysiology 25, no 6 (1995) : 348–53. http://dx.doi.org/10.1007/bf01053210.

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Johnson, Stephen M., Julia E. R. Wilkerson, Michael R. Wenninger, Daniel R. Henderson et Gordon S. Mitchell. « Role of synaptic inhibition in turtle respiratory rhythm generation ». Journal of Physiology 544, no 1 (octobre 2002) : 253–65. http://dx.doi.org/10.1113/jphysiol.2002.019687.

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Duffin, J., K. Ezure et J. Lipski. « Breathing Rhythm Generation : Focus on the Rostral Ventrolateral Medulla ». Physiology 10, no 3 (1 juin 1995) : 133–40. http://dx.doi.org/10.1152/physiologyonline.1995.10.3.133.

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Current knowledge about the generation of breathing rhythm is reviewed. The respiratory neurophysiology of the medulla and particularly its rostral ventrolateral part as well as the major hypotheses of breathing rhythm generation are discussed. A model incorporating recent concepts is presented.
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Thoby-Brisson, Muriel. « Neural mechanisms for sigh generation during prenatal development ». Journal of Neurophysiology 120, no 3 (1 septembre 2018) : 1162–72. http://dx.doi.org/10.1152/jn.00314.2018.

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The respiratory network of the preBötzinger complex (preBötC), which controls inspiratory behavior, can in normal conditions simultaneously produce two types of inspiration-related rhythmic activities: the eupneic rhythm composed of monophasic, low-amplitude, and relatively high-frequency bursts, interspersed with sigh rhythmic activity, composed of biphasic, high-amplitude, and lower frequency bursts. By combining electrophysiological recordings from transverse brainstem slices with computational modeling, new advances in the mechanisms underlying sigh production have been obtained during prenatal development. The present review summarizes recent findings that establish when sigh rhythmogenesis starts to be produced during embryonic development as well as the cellular, membrane, and synaptic properties required for its expression. Together, the results demonstrate that although generated by the same network, the eupnea and sigh rhythms have different developmental onset times and rely on distinct network properties. Because sighs (also known as augmented breaths) are important in maintaining lung function (by reopening collapsed alveoli), gaining insight into their underlying neural mechanisms at early developmental stages is likely to help in the treatment of prematurely born babies often suffering from breathing deficiencies.
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Elsen, Frank P., et Jan-Marino Ramirez. « Postnatal Development Differentially Affects Voltage-Activated Calcium Currents in Respiratory Rhythmic Versus Nonrhythmic Neurons of the Pre-Bötzinger Complex ». Journal of Neurophysiology 94, no 2 (août 2005) : 1423–31. http://dx.doi.org/10.1152/jn.00237.2005.

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The mammalian respiratory network reorganizes during early postnatal life. We characterized the postnatal developmental changes of calcium currents in neurons of the pre-Bötzinger complex (pBC), the presumed site for respiratory rhythm generation. The pBC contains not only respiratory rhythmic (R) but also nonrhythmic neurons (nR). Both types of neurons express low- and high-voltage-activated (LVA and HVA) calcium currents. This raises the interesting issue: do calcium currents of the two co-localized neuron types have similar developmental profiles? To address this issue, we used the whole cell patch-clamp technique to compare in transverse slices of mice LVA and HVA calcium current amplitudes of the two neuron populations (R and nR) during the first and second postnatal week (P0–P16). The amplitude of HVA currents did not significantly change in R pBC-neurons (P0–P16), but it significantly increased in nR pBC-neurons during P8–P16. The dehydropyridine (DHP)-sensitive current amplitudes did not significantly change during the early postnatal development, suggesting that the observed amplitude changes in nR pBC-neurons are caused by (DHP) insensitive calcium currents. The ratio between HVA calcium current amplitudes dramatically changed during early postnatal development: At P0–P3, current amplitudes were significantly larger in R pBC-neurons, whereas at P8–P16, current amplitudes were significantly larger in nR pBC-neurons. Our results suggest that calcium currents in pBC neurons are differentially altered during postnatal development and that R pBC-neurons have fully expressed calcium currents early during postnatal development. This may be critical for stable respiratory rhythm generation in the underlying rhythm generating network.
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Johnson, Stephen M., Liana M. Wiegel et David J. Majewski. « Are pacemaker properties required for respiratory rhythm generation in adult turtle brain stems in vitro ? » American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no 2 (août 2007) : R901—R910. http://dx.doi.org/10.1152/ajpregu.00912.2006.

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The role of pacemaker properties in vertebrate respiratory rhythm generation is not well understood. To address this question from a comparative perspective, brain stems from adult turtles were isolated in vitro, and respiratory motor bursts were recorded on hypoglossal (XII) nerve rootlets. The goal was to test whether burst frequency could be altered by conditions known to alter respiratory pacemaker neuron activity in mammals (e.g., increased bath KCl or blockade of specific inward currents). While bathed in artificial cerebrospinal fluid (aCSF), respiratory burst frequency was not correlated with changes in bath KCl (0.5–10.0 mM). Riluzole (50 μM; persistent Na+ channel blocker) increased burst frequency by 31 ± 5% ( P < 0.05) and decreased burst amplitude by 42 ± 4% ( P < 0.05). In contrast, flufenamic acid (FFA, 20–500 μM; Ca2+-activated cation channel blocker) reduced and abolished burst frequency in a dose- and time-dependent manner ( P < 0.05). During synaptic inhibition blockade with bicuculline (50 μM; GABAA channel blocker) and strychnine (50 μM; glycine receptor blocker), rhythmic motor activity persisted, and burst frequency was directly correlated with extracellular KCl (0.5–10.0 mM; P = 0.005). During synaptic inhibition blockade, riluzole (50 μM) did not alter burst frequency, whereas FFA (100 μM) abolished burst frequency ( P < 0.05). These data are most consistent with the hypothesis that turtle respiratory rhythm generation requires Ca2+-activated cation channels but not pacemaker neurons, which thereby favors the group-pacemaker model. During synaptic inhibition blockade, however, the rhythm generator appears to be transformed into a pacemaker-driven network that requires Ca2+-activated cation channels.
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Funk, G. D., S. M. Johnson, J. C. Smith, X. W. Dong, J. Lai et J. L. Feldman. « Functional Respiratory Rhythm Generating Networks in Neonatal Mice Lacking NMDAR1 Gene ». Journal of Neurophysiology 78, no 3 (1 septembre 1997) : 1414–20. http://dx.doi.org/10.1152/jn.1997.78.3.1414.

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Funk, G. D., S. M. Johnson, J. C. Smith, X.-W. Dong, J. Lai, and J. L. Feldman. Functional respiratory rhythm generating networks in neonatal mice lacking NMDAR1 gene. J. Neurophysiol. 78: 1414–1420, 1997. N-methyl-d-aspartate (NMDA) receptor-mediated synaptic transmission is implicated in activity-dependent developmental reorganization in mammalian brain, including sensory systems and spinal motoneuron circuits. During normal development, synaptic interactions important in activity-dependent modification of neuronal circuits may be driven spontaneously ( Shatz 1990b ). The respiratory system exhibits substantial spontaneous activity in utero; this activity may be critical in assuring essential and appropriate breathing movements from birth. We tested the hypothesis that NMDA receptors are necessary for prenatal development of central neural circuits underlying respiratory rhythm generation by comparing the responsiveness of control mice and mutant mice lacking the NMDA receptor R1 subunit (NMDAR1) gene to glutamate receptor agonists and antagonists and comparing endogenous respiratory-related oscillations generated in vitro by brain stem-spinal cord and medullary slice preparations from control and mutant mice. In control mice, local application of NMDA and the non-NMDA receptor agonist, (R,S)-α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid hydrobromide (AMPA), over the pre-Bötzinger Complex, the C4 cervical motor neuron pool, and the hypoglossal motor nucleus produced profound increases in inspiratory frequency, tonic discharge on C4 ventral nerve roots, and inward currents in inspiratory hypoglossal motoneurons, respectively. Responses of mutant mice to AMPA were similar. However, mutant mice were completely unresponsive to NMDA applications. Preparations from mutant mice generated a respiratory rhythm virtually identical to control. Results demonstrate that NMDA receptors are not essential for respiratory rhythm generation or drive transmission in the neonate. More importantly, they suggest that NMDA receptors are not obligatory for the prenatal development of circuits producing respiratory rhythm.
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Garcia, Alfredo J., Naama Rotem-Kohavi, Atsushi Doi et Jan-Marino Ramirez. « Post-Hypoxic Recovery of Respiratory Rhythm Generation Is Gender Dependent ». PLoS ONE 8, no 4 (8 avril 2013) : e60695. http://dx.doi.org/10.1371/journal.pone.0060695.

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McCrimmon, Donald R., Armelle Monnier, Fumiaki Hayashi et Edward J. Zuperku. « Pattern Formation And Rhythm Generation In The Ventral Respiratory Group ». Clinical and Experimental Pharmacology and Physiology 27, no 1-2 (janvier 2000) : 126–31. http://dx.doi.org/10.1046/j.1440-1681.2000.03193.x.

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Paton, Julian F. R., Ana P. L. Abdala, Hidehiko Koizumi, Jeffrey C. Smith et Walter M. St-John. « Respiratory rhythm generation during gasping depends on persistent sodium current ». Nature Neuroscience 9, no 3 (12 février 2006) : 311–13. http://dx.doi.org/10.1038/nn1650.

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Muñoz-Ortiz, J., E. Muñoz-Ortiz, L. López-Meraz, L. Beltran-Parrazal et C. Morgado-Valle. « The pre-Bötzinger complex : Generation and modulation of respiratory rhythm ». Neurología (English Edition) 34, no 7 (septembre 2019) : 461–68. http://dx.doi.org/10.1016/j.nrleng.2018.05.006.

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Chatonnet, Fabrice, Muriel Thoby-Brisson, Véronique Abadie, Eduardo Domı́nguez del Toro, Jean Champagnat et Gilles Fortin. « Early development of respiratory rhythm generation in mouse and chick ». Respiratory Physiology & ; Neurobiology 131, no 1-2 (juillet 2002) : 5–13. http://dx.doi.org/10.1016/s1569-9048(02)00033-2.

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Greer, John J., Jo Ellen Carter et Douglas W. Allan. « Respiratory rhythm generation in a precocial rodent in vitro preparation ». Respiration Physiology 103, no 2 (février 1996) : 105–12. http://dx.doi.org/10.1016/0034-5687(95)00073-9.

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Baghdadwala, Mufaddal I., Maryana Duchcherer, Jenny Paramonov et Richard J. A. Wilson. « Three brainstem areas involved in respiratory rhythm generation in bullfrogs ». Journal of Physiology 593, no 13 (17 juin 2015) : 2941–54. http://dx.doi.org/10.1113/jp270380.

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Fortin, Gilles, Patrick Charnay et Jean Champagnat. « Linking respiratory rhythm generation to segmentation of the vertebrate hindbrain ». Pflügers Archiv - European Journal of Physiology 446, no 5 (1 mai 2003) : 514–15. http://dx.doi.org/10.1007/s00424-003-1083-2.

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Garcia, Alfredo J., Jean Charles Viemari et Maggie A. Khuu. « Respiratory rhythm generation, hypoxia, and oxidative stress—Implications for development ». Respiratory Physiology & ; Neurobiology 270 (décembre 2019) : 103259. http://dx.doi.org/10.1016/j.resp.2019.103259.

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De Oliveira, Renato, et Chris Fietkiewicz. « Nonlinear variability in a computational model of respiratory rhythm generation ». Journal of Critical Care 28, no 1 (février 2013) : e10. http://dx.doi.org/10.1016/j.jcrc.2012.10.035.

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Eldridge, F. L., D. Paydarfar, P. G. Wagner et R. T. Dowell. « Phase resetting of respiratory rhythm : effect of changing respiratory "drive" ». American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no 2 (1 août 1989) : R271—R277. http://dx.doi.org/10.1152/ajpregu.1989.257.2.r271.

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We studied the effect of changing drive on resetting of respiratory rhythm in anesthetized cats and in a model (Van der Pol) of a limit-cycle oscillator. In cats, rhythm was perturbed by brief mesencephalic stimuli. Stimulus time in the cycle (old phases) and times of onset of rescheduled breaths (cophases) were measured. Previous study [Paydarfar and Eldridge, Am. J. Physiol. 252 (Regulatory Integrative Comp. Physiol. 21): R55-R62, 1987] showed distinct types of phase resetting that depended on strength of stimuli. In this study, stimulus strength was kept constant, but respiratory drive was changed by increasing PCO2, by stimulating carotid sinus nerve, or by cooling intermediate areas of ventral medulla. Type 0 (strong) resetting occurred when respiratory drive was low, type 1 (weak) resetting when drive was high, and a phase singularity when drive was intermediate. Phase-resetting patterns generated by the model showed the same behavior when a drive parameter was changed. The findings support the idea that continuous limit-cycle dynamics underlie generation of respiratory rhythm. Increased respiratory drive, by increasing size of the limit cycle, reduces functional effectiveness of the same perturbing stimulus in causing phase resetting.
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Ramirez, Jan-Marino, et Nathan A. Baertsch. « The Dynamic Basis of Respiratory Rhythm Generation : One Breath at a Time ». Annual Review of Neuroscience 41, no 1 (8 juillet 2018) : 475–99. http://dx.doi.org/10.1146/annurev-neuro-080317-061756.

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Rhythmicity is a universal timing mechanism in the brain, and the rhythmogenic mechanisms are generally dynamic. This is illustrated for the neuronal control of breathing, a behavior that occurs as a one-, two-, or three-phase rhythm. Each breath is assembled stochastically, and increasing evidence suggests that each phase can be generated independently by a dedicated excitatory microcircuit. Within each microcircuit, rhythmicity emerges through three entangled mechanisms: ( a) glutamatergic transmission, which is amplified by ( b) intrinsic bursting and opposed by ( c) concurrent inhibition. This rhythmogenic triangle is dynamically tuned by neuromodulators and other network interactions. The ability of coupled oscillators to reconfigure and recombine may allow breathing to remain robust yet plastic enough to conform to nonventilatory behaviors such as vocalization, swallowing, and coughing. Lessons learned from the respiratory network may translate to other highly dynamic and integrated rhythmic systems, if approached one breath at a time.
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Haouzi, Philippe, et Harold J. Bell. « Control of breathing and volitional respiratory rhythm in humans ». Journal of Applied Physiology 106, no 3 (mars 2009) : 904–10. http://dx.doi.org/10.1152/japplphysiol.90675.2008.

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When breathing frequency (f) is imperceptibly increased during a volitionally paced respiratory rhythm imposed by an auditory signal, tidal volume (Vt) decreases such that minute ventilation (V̇e) rises according to f-induced dead-space ventilation changes ( 18 ). As a result, significant change in alveolar ventilation and Pco2 are prevented as f varies. The present study was performed to determine what regulatory properties are retained by the respiratory control system, wherein the spontaneous automatic rhythmic activity is replaced by a volitionally paced rhythm. Six volunteers were asked to trigger each breath cycle on hearing a brief auditory signal. The time interval between subsequent auditory signals was imperceptibly changed for 10–15 min, during 1) air breathing ( condition 1), 2) the addition of a 300 ml of instrumental dead space ( condition 2), 3) an increase in the inspired level of CO2 ( condition 3), and 4) light exercise ( condition 4). We found that as f was slowly increased the elaborated Vt decreased in accordance to the background level of CO2 and metabolic rate. Indeed, for any given breath duration, Vt was shifted upward in condition 2 vs. 1, whereas the slope of Vt changes according to the volitionally rhythm was much steeper in conditions 3 and 4 vs. 1. The resulting changes in V̇e offset any f-induced changes in dead-space ventilation in all conditions. We conclude that there is an inherent, fundamental mechanism that elaborates Vt based on f when imposed by the premotor cortex in humans. The chemoreflex and exercise drive to breath interacts with this cortically mediated rhythm maintaining alveolar rather than V̇e constant as f changes. The implications of our findings are discussed in the context of our current understanding of the central generation of breathing rhythm.
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Shao, Xuesi M., et Jack L. Feldman. « Respiratory Rhythm Generation and Synaptic Inhibition of Expiratory Neurons in Pre-Bötzinger Complex : Differential Roles of Glycinergic and GABAergic Neural Transmission ». Journal of Neurophysiology 77, no 4 (1 avril 1997) : 1853–60. http://dx.doi.org/10.1152/jn.1997.77.4.1853.

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Shao, Xuesi M. and Jack L. Feldman. Respiratory rhythm generation and synaptic inhibition of expiratory neurons in pre-Bötzinger complex: differential roles of glycinergic and GABAergic neural transmission. J. Neurophysiol. 77: 1853–1860, 1997. A key distinction between neural pacemaker and conventional network models for the generation of breathing rhythm in mammals is whether phasic reciprocal inhibitory interactions between inspiratory and expiratory neurons are required. In medullary slices from neonatal rats generating respiratory-related rhythm, we measured the phasic inhibitory inputs to expiratory neurons with the use of whole cell patch clamp in the hypothesized rhythm generation site, the pre-Bötzinger complex (pre-BötC). Expiratory neurons, which generate tonic impulse activity during the expiratory period, exhibited inhibitory postsynaptic potentials (IPSPs) synchronized to the periodic inspiratory bursts of the hypoglossal nerve root (XIIn). Bath application of the glycine receptor antagonist strychnine (STR; 5–10 μM) reversibly blocked these inspiratory-phase IPSPs, whereas the γ-aminobutyric acid-A (GABAA) receptor antagonist bicuculline (BIC; 10–100 μM) had no effect on these IPSPs. Replacing the control in vitro bathing solution with a Cl−-free solution also abolished these IPSPs. Respiratory-related rhythmic activity was not abolished when inspiratory-phase IPSPs were blocked. The frequency and strength of XIIn rhythmic activity increased and seizurelike activity was produced when either STR, BIC, or Cl−-free solution was applied. Inspiratory-phase IPSPs were stable after establishment of whole cell patch conditions (patch pipettes contained 7 mM Cl−). Under voltage clamp, the reversal potential of inspiratory-phase inhibitory postsynaptic currents (IPSCs) was −75 mV. The current-voltage ( I- V) curve for IPSCs shifted to the right when extracellular Cl− concentration was reduced by 50% (70 mM) and the reversal potential was reduced to −60 mV, close to the new Cl− Nernst potential. In tetrodotoxin (0.5 μM) under voltage clamp (holding potential = −45 mV), local application of glycine (1 mM) over pre-BötC induced an outward current and an increase in membrane conductance in expiratory neurons. The effect was blocked by bath application of STR (0.8–1 μM). Local application of the GABAA receptor agonist 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP, 1 mM) induced an outward current and an increase in membrane conductance that was blocked by BIC (10–100 mM). Under voltage clamp (holding potential = −45 mV), we analyzed spontaneous IPSCs during expiration in expiratory neurons. Bath application of BIC (10 μM) reduced the IPSC frequency (from 2.2 to 0.3 per s), whereas the inspiratory-phase IPSCs did not change. Bath application of STR (8–10 μM) abolished both IPSCs. These results indicate that 1) reciprocal inhibition of expiratory neurons is glycinergic and mediated by a glycine-activated Cl− channel that is not required for respiratory-related rhythm generation in neonatal rat medullary slices; 2) endogenous GABA and glycine modulate the excitability of respiratory neurons and affect respiratory pattern in the slice preparation; 3) both glycine and GABAA receptors are found on pre-BötC expiratory neurons, and these receptors are sensitive to STR and BIC, respectively; 4) glycine and GABAA inhibitory mechanisms play different functional roles in expiratory neurons: both glycine and GABAA receptors modulate neuronal excitability, whereas glycinergic transmission alone is responsible for reciprocal inhibition; and 5) intracellular Cl− concentration in these neonatal expiratory neurons is similar to that in adults.
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Mellen, Nicholas M., Wiktor A. Janczewski, Christopher M. Bocchiaro et Jack L. Feldman. « Opioid-Induced Quantal Slowing Reveals Dual Networks for Respiratory Rhythm Generation ». Neuron 37, no 5 (mars 2003) : 821–26. http://dx.doi.org/10.1016/s0896-6273(03)00092-8.

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