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13 results on '"Eugene Nattie"'

1. Acute perturbation of Pet1-neuron activity in neonatal mice impairs cardiorespiratory homeostatic recovery

Author

Ryan T Dosumu-Johnson, Andrea E Cocoran, YoonJeung Chang, Eugene Nattie, and Susan M Dymecki

Subjects
autoresuscitation, neonatal, raphe, serotonergic system, chemogenetics, SIDS, Medicine, Science, Biology (General), QH301-705.5
Abstract

Cardiorespiratory recovery from apneas requires dynamic responses of brainstem circuitry. One implicated component is the raphe system of Pet1-expressing (largely serotonergic) neurons, however their precise requirement neonatally for homeostasis is unclear, yet central toward understanding newborn cardiorespiratory control and dysfunction. Here we show that acute in vivo perturbation of Pet1-neuron activity, via triggering cell-autonomously the synthetic inhibitory receptor hM4Di, resulted in altered baseline cardiorespiratory properties and diminished apnea survival. Respiratory more than heart rate recovery was impaired, uncoupling their normal linear relationship. Disordered gasp recovery from the initial apnea distinguished mice that would go on to die during subsequent apneas. Further, the risk likelihood of apnea-related mortality associated with suppression of Pet1 neurons was higher for animals with baseline elevated ventilatory equivalents for oxygen. These findings establish that Pet1 neurons play an active role in neonatal cardiorespiratory homeostasis and provide mechanistic plausibility for the serotonergic abnormalities associated with SIDS.

Published
2018
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2. Functional and Developmental Identification of a Molecular Subtype of Brain Serotonergic Neuron Specialized to Regulate Breathing Dynamics

Author

Rachael D. Brust, Andrea E. Corcoran, George B. Richerson, Eugene Nattie, and Susan M. Dymecki

Subjects
Biology (General), QH301-705.5
Abstract

Serotonergic neurons modulate behavioral and physiological responses from aggression and anxiety to breathing and thermoregulation. Disorders involving serotonin (5HT) dysregulation are commensurately heterogeneous and numerous. We hypothesized that this breadth in functionality derives in part from a developmentally determined substructure of distinct subtypes of 5HT neurons each specialized to modulate specific behaviors. By manipulating developmentally defined subgroups one by one chemogenetically, we find that the Egr2-Pet1 subgroup is specialized to drive increased ventilation in response to carbon dioxide elevation and acidosis. Furthermore, this subtype exhibits intrinsic chemosensitivity and modality-specific projections—increasing firing during hypercapnic acidosis and selectively projecting to respiratory chemosensory but not motor centers, respectively. These findings show that serotonergic regulation of the respiratory chemoreflex is mediated by a specialized molecular subtype of 5HT neuron harboring unique physiological, biophysical, and hodological properties specified developmentally and demonstrate that the serotonergic system contains specialized modules contributing to its collective functional breadth.

Published
2014
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3. The role of melanin concentrating hormone (MCH) in the central chemoreflex: a knockdown study by siRNA in the lateral hypothalamus in rats.

Author

Ningjing Li, Eugene Nattie, and Aihua Li

Subjects
Medicine, Science
Abstract

Melanin concentrating hormone (MCH), a neuropeptide produced mainly in neurons localized to the lateral hypothalamic area (LHA), has been implicated in the regulation of food intake, energy balance, sleep state, and the cardiovascular system. Hypothalamic MCH neurons also have multisynaptic connections with diaphragmatic motoneurons and project to many central chemoreceptor sites. However, there are few studies of MCH involvement in central respiratory control. To test the hypothesis that MCH plays a role in the central chemoreflex, we induced a down regulation of MCH in the central nervous system by knocking down the MCH precursor (pMCH) mRNA in the LHA using a pool of small interfering RNA (siRNA), and measured the resultant changes in breathing, metabolic rate, body weight, and blood glucose levels in conscious rats. The injections of pMCH-siRNA into the LHA successfully produced a ∼ 62% reduction of pMCH mRNA expression in the LHA and a ∼ 43% decrease of MCH levels in the cerebrospinal fluid relative to scrambled-siRNA treatment (P = 0.006 and P = 0.02 respectively). Compared to the pretreatment baseline and the scrambled-siRNA treated control rats, knockdown of MCH resulted in: 1) an enhanced hypercapnic chemoreflex (∼ 42 & 47% respectively; P < 0.05) only in wakefulness; 2) a decrease in body weight and basal glucose levels; and 3) an unchanged metabolic rate. Our results indicate that MCH participates not only in the regulation of glucose and sleep-wake homeostasis but also the vigilance-state dependent regulation of the central hypercapnic chemoreflex and respiratory control.

Published
2014
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4. Pre- and early postnatal nicotine exposure exacerbates autoresuscitation failure in serotonin-deficient rat neonates

Author

Stella Y, Lee, Chrystelle M, Sirieix, Eugene, Nattie, and Aihua, Li

Subjects
Male, Medulla Oblongata, Nicotine, Serotonin, Respiration, Research Papers, Rats, Sprague-Dawley, Animals, Newborn, Pregnancy, Animals, Female, Cotinine, Hypoxia, Maternal-Fetal Exchange
Abstract

KEY POINTS: Sudden infant death syndrome (SIDS) is one of the leading causes of death during the first year of life and abnormalities linked to serotonin (5‐HT) have been identified in many SIDS cases. Cigarette smoking and associated exogenous stressors, e.g. developmental nicotine exposure, may compound these serotonergic defects and any associated defects in cardiorespiratory function. Using neonatal rodent pups subjected to medullary 5‐HT deficiency and perinatal nicotine exposure, we examined the impact of this interplay of factors on the neonates’ ability to autoresuscitate at specific ages. In perinatal nicotine‐exposed 5‐HT deficient pups, impaired autoresuscitation along with significantly delayed post‐anoxic recovery of normal breathing and heart rate was observed at postnatal day 10 (P10). We found that the interaction between 5‐HT deficiency and perinatal nicotine exposure can significantly increase pups’ vulnerability to environmental stressors and exacerbate defects in cardiorespiratory protective reflexes to repetitive anoxia during the development period. ABSTRACT: Cigarette smoking during pregnancy increases the risk of sudden infant death syndrome (SIDS), and nicotine replacements, a key ingredient of cigarettes, have been recently prescribed to women who wish to quit smoking during their pregnancy. Serotonin (5‐HT) abnormalities have been consistently identified in many SIDS cases. Here we investigated the effects of perinatal nicotine exposure in mild 5‐HT deficiency rat neonates on autoresuscitation, a protective cardiorespiratory reflex. The mild 5‐HT deficiency was induced by a maternal tryptophan‐deficient diet, and nicotine was delivered from embryonic day (E) 4 to postnatal day (P) 10 at 6 mg kg(−1) day(−1) through an osmotic pump. In P10 rats, nicotine exposure exacerbates autoresuscitation failure (mortality) in mildly 5‐HT‐deficient rats to a greater extent than in controls (P = 0.029). The recovery of eupnoea and heart rate to baseline values following repetitive anoxic events (which elicit an apnoea accompanied by a bradycardia) is significantly delayed in 5‐HT‐deficient rats treated with nicotine, making them more susceptible to failure of autoresuscitation (eupnoea recovery: P = 0.0053; heart rate recovery: P =

Published
2018

5. Ondine Undone

Author

Eugene Nattie

Subjects
Mice, Knockout, Mice, Potassium Channels, Tandem Pore Domain, Respiration, Animals, Humans, General Medicine, Hypoventilation, Carbon Dioxide, Sleep Apnea, Central, Receptors, G-Protein-Coupled
Published
2015

6. Focal microdialysis of CO₂ in the perifornical-hypothalamic area increases ventilation during wakefulness but not NREM sleep

Author

Ningjing, Li, Aihua, Li, and Eugene, Nattie

Subjects
Male, Analysis of Variance, Electromyography, Microdialysis, Hypothalamus, Prefrontal Cortex, Electroencephalography, Carbon Dioxide, Article, Rats, Rats, Sprague-Dawley, Neural Pathways, Animals, Sleep Stages, Wakefulness, Pulmonary Ventilation
Abstract

We investigated whether the perifornical-lateral hypothalamic area (PF-LHA), where the orexin neurons reside, is a central chemoreceptor site by microdialysis of artificial cerebrospinal fluid (aCSF) equilibrated with 25% CO(2) into PF-LHA in conscious rats. This treatment is known to produce a focal tissue acidification like that associated with a 6-7 mm Hg increase in arterial [Formula: see text] . Such focal acidification in the PF-LHA significantly increased ventilation up to 15% compared with microdialysis of normal aCSF equilibrated with 5% CO(2) only in wakefulness but not in sleep in both the dark (P=0.004) and light (P0.001) phases of the diurnal cycle. This response was predominantly due to a significant increase in respiratory frequency (11%, P0.001). There were no significant effects on ventilation in the group with probes misplaced outside the PF-LHA. These results suggest that PF-LHA functions as a central chemoreceptor site in the central nervous system in a vigilant state dependent manner with predominant effects in wakefulness.

Published
2012

7. List of Contributors

Author

Mauro Abbate, Horacio J. Adrogué, Seth L. Alper, Robert J. Alpern, Radhakrishna Baliga, Daniel Batlle, José F. Bernardo, Theresa J. Berndt, Mark O. Bevensee, Jürg Biber, René J.M. Bindels, Henrik Birn, Walter F. Boron, D. Craig Brater, Edward M. Brown, Gerhard Burckhardt, Simone M.R. Camargo, Michael J. Caplan, Andrés Cárdenas, Sheldon Chen, Erik Ilsø Christensen, Moonja Chung-Park, Fredric L. Coe, Kirk P. Conrad, Christopher J. Cooper, Norman P. Curthoys, Prasad Devarajan, Matthew Diamond, Cristina Dumitru, Lance D. Dworkin, Kai-Uwe Eckardt, Zoltán Huba Endre, Andrew Evan, Ronald J. Falk, Ian C. Forster, Peter A. Friedman, Clarice Kazue Fujihara, John P. Geibel, Kathleen M. Giacomini, Pere Ginès, Simin Goral, Mitchell Halperin, L. Lee Hamm, Syed K. Haque, Steven C. Hebert, J. Harold Helderman, William L. Henrich, Nati Hernando, Joost G.J. Hoenderop, Jonathon W. Homeister, Charles S. Hummel, J. Charles Jennette, Kamel S. Kamel, S. Ananth Karumanchi, Clifford E. Kashtan, Charbel Khoury, Robert Kleta, Hermann Koepsell, Martin Konrad, Reto Krapf, Rajiv Kumar, Armin Kurtz, Ira Kurtz, Anthony J. Langone, Shih-Hua Lin, Marshall D. Lindheimer, Christopher Y. Lu, Daniela Macconi, Michael Madaio, Nicolaos E. Madias, Victoria Makrides, Anup Manoharon, Pär Matsson, William E. Mitch, Orson W. Moe, Bruce A. Molitoris, Heini Murer, Eugene Nattie, Rikke Nielsen, Biff F. Palmer, Patricia A. Preisig, Gary A. Quamme, L. Darryl Quarles, Mohan Rajapurkar, Giuseppe Remuzzi, Daniela Riccardi, Heidi Schaefer, Jeffrey R. Schelling, Karl P. Schlingmann, Robert W. Schrier, John R. Sedor, Yoav Segal, Donald W. Seldin, Sudhir V. Shah, Asif Sharfuddin, Stefan Somlo, Andrew K. Stewart, Peter J. Tebben, Vicente E. Torres, François Verrey, Robert James Walker, Roland H. Wenger, Elaine Worcester, Biruh T. Workeneh, Ernest M. Wright, John Wysolmerski, Sung-Sen Yang, Roberto Zatz, Fuad N. Ziyadeh, and Carla Zoja

Published
2012

8. C

Author

Justin R. Davis, Andrew C. Giles, Catharine H. Rankin, Jonathan Bell, Hiroshi Kimura, Tadashi Uemura, Yoshi Kidokoro, Mado Lemieux, Paul De Koninck, Emilio Carbone, Adriano Senatore, J. David Spafford, Megan J. Dowie, Natasha L. Grimsey, Michelle Glass, Kevin D. Gillis, Peter Hunter, Brian Budgell, Arijit Roy, Richard J. A. Wilson, Okihide Hikosaka, Michael Esfeld, Jens Harbecke, Takayuki Mitsuhashi, Takao Takahashi, Ryoichiro Kageyama, Ryosuke Ohsawa, Toshiyuki Ohtsuka, Peter M. Lalley, Michael N. Nitabach, Julian F. R. Paton, David M. Waitzman, Eugene Nattie, Aihua Li, Ikuo Tsunoda, Mikako Kobayashi-Warren, Jane E. Libbey, Robert S. Fujinami, Amod P. Kulkarni, Laurie A. Kellaway, Girish J. Kotwal, Katrin E. Morgen, Maria Grazia Ciufolini, Loredana Nicoletti, Randall L. Davis, Markus J. Hofer, Iain L. Campbell, Troels S. Jensen, Nanna B. Finnerup, Volko A. Straub, Eduardo E. Benarroch, Adolfo M. Bronstein, Antoine Nissant, James R. Bloedel, Vlastislav Bracha, Stephen M. Highstein, Charles A. Scudder, Torah M. Kachur, Dave B. Pilgrim, Holley André, Joseph A. Mindell, Merritt Maduke, John Ormond, Melanie A. Woodin, Subimal Datta, David D. Eisenstat, Kaare Severinsen, Johannes Jakobsen, Martha Merrow, Till Roenneberg, Jeffrey D. Schall, Brent A. Vogt, Robert J. Morecraft, Shelley Tischkau, Menno P. Gerkema, Ruud M. Buijs, Alfred J. Lewy, David Hazlerigg, Takashi Yamamoto, Marcelo Epstein, Jürgen A. Ripperger, Urs Albrecht, Achim Kramer, Mario A. Ruggero, Robert V. Shannon, Manuel S. Malmierca, Philip H. Smith, Beate Sodian, Andreas Nieder, Fred W. Mast, Ben Godde, Thorsten Hansen, Karl R. Gegenfurtner, Philippe Faure, Douglas W. Allan, Hideki Asoh, Wilfrid Jänig, Ilya A. Rybak, Jeffrey C. Smith, Amir Karniel, Vittorio Sanguineti, Fiona Mansergh, Jonathan R.Wolpaw, Dennis J. McFarland, Denis Mareschal, Nadja Althaus, Tai Sing Lee, Thomas A. Cleland, Graham C. Goodwin, Arie Feuer, Mark L. Latash, Oscar Marín, Paul J. Lucassen, Karin Boekhoorn, Fiona Francis, Henk J. Groenewegen, Hisashi Ogawa, Vaughan G Macefield, Ingvars Birznieks, and Martin Biel

Published
2009

10. Contributors

Author

MAURO ABBATE, DALE R. ABRAHAMSON, MARCIN ADAMCZAK, HORACIO J. ADROGUÉ, SETH L. ALPER, ROBERT J. ALPERN, THOMAS E. ANDREOLI, ANITA C. APERIA, MATTHEW A. BAILEY, DANIEL BATLLE, MICHEL BAUM, THERESA J. BERNDT, MARK O. BEVENSEE, JÜRG BIBER, DANIEL G. BICHET, RENÉ J.M. BINDELS, ROLAND C. BLANTZ, WALTER F. BORON, D. CRAIG BRATER, JOSEPHINE P. BRIGGS, ALEX BROWN, NIGEL J. BRUNSKILL, GERHARD BURCKHARDT, GEOFFREY BURNSTOCK, LLOYD CANTLEY, CHUNHUA CAO, GIOVAMBATTISTA CAPASSO, MICHAEL J. CAPLAN, HUGH J. CARROLL, LAURENCE CHAN, MOONJA CHUNG-PARK, FREDRIC L. COE, THOMAS M. COFFMAN, WAYNE D. COMPER, KIRK P. CONRAD, STEVEN D. CROWLEY, NORMAN P. CURTHOYS, PEDRO R. CUTILLAS, THEODORE M. DANOFF, EDWARD S. DEBNAM, HENRIK DIMKE, ALAIN DOUCET, RAGHVENDRA K. DUBEY, ADRIANA DUSSO, KAI-UWE ECKARDT, DAVID H. ELLISON, HITOSHI ENDOU, ZOLTÁN HUBA ENDRE, FRANKLIN H. EPSTEIN, ANDREW EVAN, RONALD J. FALK, KAMBIZ FARBAKHSH, NICHOLAS R. FERRERI, PEYING FONG, MANASSES CLAUDINO FONTELES, IAN FORSTER, LEONARD RALPH FORTE, HAROLD A. FRANCH, LYNDA A. FRASSETTO, PETER A. FRIEDMAN, JØRGEN FRØKLÆR, JOHN P. GEIBEL, MICHAEL GEKLE, GERHARD GIEBISCH, PERE GINÈS, STEVE A.N. GOLDSTEIN, SIMIN GORAL, SIAN V. GRIFFIN, WILLIAM B. GUGGINO, THERESA A. GUISE, SUSAN B. GURLEY, STEPHEN D. HALL, MITCHELL L. HALPERIN, L. LEE HAMM, STEVEN C. HEBERT, MATTHIAS A. HEDIGER, J. HAROLD HELDERMAN, WILLIAM L. HENRICH, AILLEEN HERAS-HERZIG, NATI HERNANDO, JOOST G.J. HOENDEROP, ULLA HOLTBÄCK, JEAN-DANIEL HORISBERGER, EDITH HUMMLER, TRACY E. HUNLEY, EDWIN K. JACKSON, J. CHARLES JENNETTE, EDWARD J. JOHNS, JOHN P. JOHNSON, BRIGITTE KAISSLING, KAMEL S. KAMEL, S. ANANTH KARUMANCHI, CLIFFORD E. KASHTAN, BERTRAM L. KASISKE, ADRIAN I. KATZ, BRIAN F. KING, SAULO KLAHR, THOMAS R. KLEYMAN, HERMANN KOEPSELL, VALENTINA KON, MARTIN KONRAD, ULLA C. KOPP, RETO KRAPF, WILHELM KRIZ, RAJIV KUMAR, CHRISTINE E. KURSCHAT, ARMIN KURTZ, TAE-HWAN KWON, CHRISTOPHER P. LANDOWSKI, ANTHONY J. LANGONE, FLORIAN LANG, HAROLD E. LAYTON, THU H. LE, DANIEL I. LEVY, SHIH-HUA LIN, MARSHALL D. LINDHEIMER, CHRISTOPHER Y. LU, MICHAEL P. MADAIO, NICOLAOS E. MADIAS, GERHARD MALNIC, KARL S. MATLIN, WILLIAM C. McCLELLAN, JOHN C. MCGIFF, C. CHARLES MICHEL, JEFFREY H. MINER, WILLIAM E. MITCH, HIROKI MIYAZAKI, ORSON W. MOE, BRUCE A. MOLITORIS, R. CURTIS MORRIS, SALIM K. MUJAIS, HEINI MURER, SHIGEAKI MUTO, EUGENE NATTIE, ERIC G. NEILSON, SØREN NIELSEN, SANJAY K. NIGAM, JOSEPH M. NOGUEIRA, MAN S. OH, MARK D. OKUSA, TANYA M. OSICKA, THOMAS L. PALLONE, BIFF F. PALMER, LAWRENCE G. PALMER, MARK D. PARKER, JOAN H. PARKS, PATRICIA A. PREISIG, GARY A. QUAMME, L. DARRYL QUARLES, RAYMOND QUIGLEY, W. BRIAN REEVES, GIUSEPPE REMUZZI, LUIS REUSS, DANIELA RICCARDI, BRIAN RINGHOFER, EBERHARD RITZ, CHRISTOPHER J. RIVARD, GARY L. ROBERTSON, ROBERT M. ROSA, BERNARD C. ROSSIER, LEILEATA M. RUSSO, HENRY SACKIN, HIROYUKI SAKURAI, JEFF M. SANDS, LISA M. SATLIN, HEIDI SCHAEFER, JEFFREY R. SCHELLING, LAURENT SCHILD, KARL P. SCHLINGMANN, JÜRGEN B. SCHNERMANN, ROBERT W. SCHRIER, ANTHONY SEBASTIAN, JOHN R. SEDOR, YOAV SEGAL, TAKASHI SEKINE, DONALD W. SELDIN, MARTIN SENITKO, MALATHI SHAH, SUDHIR V. SHAH, STUART J. SHANKLAND, ASIF A. SHARFUDDIN, KUMAR SHARMA, SHAOHU SHENG, DAVID G. SHIRLEY, STEFAN SILBERNAGL, STEPHEN M. SILVER, MEL SILVERMAN, EDUARDO SLATOPOLSKY, STEFAN SOMLO, RICHARD H. STERNS, ANDREW K. STEWART, YOSHIRO SUZUKI, PETER J. TEBBEN, SCOTT C. THOMSON, VICENTE E. TORRES, ROBERT J. UNWIN, FRANÇOIS VERREY, DAVID L. VESELY, CARSTEN A. WAGNER, MERYL WALDMAN, ROBERT JAMES WALKER, WEI WANG, WEN-HUI WANG, YINGHONG WANG, ALAN M. WEINSTEIN, PAUL A. WELLING, GUNTER WOLF, ELAINE WORCESTER, FUAD N. ZIYADEH, and CARLA ZOJA

Published
2008

11. Brainstem catecholaminergic neurons modulate both respiratory and cardiovascular function

Author

Aihua, Li, Laura, Emond, and Eugene, Nattie

Subjects
Cardiovascular Physiological Phenomena, Neurons, Catecholamines, Electromyography, Heart Rate, Respiratory Physiological Phenomena, Animals, Electroencephalography, Brain Stem, Rats
Abstract

Catecholamine neurons (CA) located in the brainstem project widely in the forebrain, hindbrain and spinal cord to many regions involved in the control of respiratory and cardiovascular function. For example, A6 noradrenergic neurons provide a tonic excitatory stimulus that maintains breathing frequency while A5 neurons provide an inhibitory influence on both cardiovascular and respiratory function to slow breathing frequency and heart rate. Mice with genetic defects that include CA neurons have abnormal respiration and blood pressure. For example, mice heterozygous for Phox2b with CA neuron defects have sleep-disordered breathing, and DBH knockout mice with absent CA cells centrally and peripherally have hypotension. Our hypothesis is that widespread brainstem CA neuron lesions in adult rats would significantly affect cardiorespiratory functions including breathing, chemoreception, blood pressure and heart rate. We produced the widespread brainstem CA neuron lesion by injecting anti-dopamine-beta-hydroxylase-saporin (DBH-SAP) via the 4th ventricle. The lesioned group had a 64-84% loss of A5, A6 and A7 tyrosine hydroxylase immunoreactive (ir) neurons along with 56-64% loss of C1 and C2 phenyl ethanolamine-N methyltransferase (PNMT)-ir neurons over 2-3 weeks. The significant respiratory changes included: (1) a decreased breathing frequency during air and 7% CO2 breathing in both wakefulness and non-REM (NREM) sleep; (2) a reduced ventilatory response to 7% CO2 in wakefulness (-28%) and in NREM sleep (-26%); and (3) increased variability of breathing in REM sleep but not in wakefulness or NREM sleep. Significant cardiovascular changes at two weeks included: (1) an increased MAP by 11.7mmHg in the room air resting condition; (2) an unaffected cardiovascular response to hypercapnia; and (3) a smaller decrease of MAP in response to hypoxia.Central CA neurons have a net excitatory effect on breathing and chemoreception but a net inhibitory effect on blood pressure.

Published
2007

12. Simultaneous inhibition of caudal medullary raphe and retrotrapezoid nucleus decreases breathing and the CO2 response in conscious rats

Author

Aihua, Li, Shawn, Zhou, and Eugene, Nattie

Subjects
Rats, Sprague-Dawley, Medulla Oblongata, nervous system, Consciousness, Respiratory Mechanics, Respiratory, Animals, Raphe Nuclei, Neural Inhibition, Carbon Dioxide, Chemoreceptor Cells, Rats
Abstract

The medullary raphe (MR) and the retrotrapezoid nucleus (RTN) in the ventral medulla are two of many central chemoreceptor sites. We examine their combined function in conscious rats by focal inhibition using microdialysis. Inhibition of RTN neurons with the GABA(A) receptor agonist muscimol, with simultaneous dialysis of artificial cerebrospinal fluid (ACSF) in or near to the caudal MR, causes hypoventilation (decrease in the ratio of minute ventilation to oxygen consumption, V(E)/V(O2)) and reduces the ventilatory response to 7% CO(2) by 24%. Inhibition of caudal MR serotonergic neurons with the 5-HT(1A) receptor agonist (R)-(+)-8-hydroxy-2(di-n-propylamino)tetralin (8-OH-DPAT), with simultaneous dialysis of ACSF in or near to the RTN, causes hypoventilation but has no significant effect on the CO(2) response. Inhibition of both the RTN and the caudal MR simultaneously produces enhanced hypoventilation and a 51% decrease in the CO(2) response. The effects of treatment on the CO(2) response are similar in wakefulness and in non-rapid eye movement sleep. Comparison of the effect of 8-OH-DPAT microdialysed into a more rostral portion of the MR, where the CO(2) response is reduced by 22%, demonstrates heterogeneity within the MR of the function of serotonergic neurons in breathing. We conclude that serotonergic neurons within the caudal MR provide a non-CO(2)-dependent tonic drive to breathe and potentiate the effects of RTN neurons that contribute to a resting chemical 'drive to breathe' as well as the response to added CO(2). These effects of caudal MR serotonergic neurons could be at a chemoreceptor site, e.g. the RTN, or at 'downstream' sites involved in rhythm and pattern generation.

Published
2006

13. Supraspinal locomotor centers do/do not contribute significantly to the hyperpnea of dynamic exercise in humans

Author

Frederick L, Eldridge, Didier, Morin, Jaroslaw Richard, Romaniuk, Stanley, Yamashiro, Jeffrey T, Potts, Ronaldo M, Ichiyama, Harold, Bell, Eliot A, Phillipson, Kieran J, Killian, Norman L, Jones, and Eugene, Nattie

Subjects
Sheep, Pulmonary Gas Exchange, Respiration, Hypothalamus, Carbon Dioxide, Motor Activity, Spinal Cord, Physical Conditioning, Animal, Subthalamus, Potassium, Respiratory Mechanics, Animals, Homeostasis, Humans, Pulmonary Ventilation, Exercise
Published
2006

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