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Medullary Respiratory Neural Activity During Hypoxia in NREM and REM Sleep in the Cat

1 Texas Tech University School of Medicine, Department of Physiology, Lubbock, Texas; 2 Information Transmission Problems Institute, Russian Academy of Science, Moscow Russia; 3 University of Wisconsin Medical School, John Rankin Laboratory of Pulmonary Medicine, Department of Population Health Scie...

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Published in:Journal of neurophysiology 2006-02, Vol.95 (2), p.803-810
Main Authors: Lovering, Andrew T, Fraigne, Jimmy J, Dunin-Barkowski, Witali L, Vidruk, Edward H, Orem, John M
Format: Article
Language:English
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Summary:1 Texas Tech University School of Medicine, Department of Physiology, Lubbock, Texas; 2 Information Transmission Problems Institute, Russian Academy of Science, Moscow Russia; 3 University of Wisconsin Medical School, John Rankin Laboratory of Pulmonary Medicine, Department of Population Health Sciences, Madison, Wisconsin; and 4 I.U.P Génie Physiologique Informatique, Université de Poitiers, Poitiers, France Submitted 13 June 2005; accepted in final form 23 September 2005 Intact unanesthetized cats hyperventilate in response to hypocapnic hypoxia in both wakefulness and sleep. This hyperventilation is caused by increases in diaphragmatic activity during inspiration and expiration. In this study, we recorded 120 medullary respiratory neurons during sleep in hypoxia. Our goal was to understand how these neurons change their activity to increase breathing efforts and frequency in response to hypoxia. We found that the response of medullary respiratory neurons to hypoxia was variable. While the activity of a small majority of inspiratory (58%) and expiratory (56%) neurons was increased in response to hypoxia, the activity of a small majority of preinspiratory (57%) neurons was decreased. Cells that were more active in hypoxia had discharge rates that averaged 183% (inspiratory decrementing), 154% (inspiratory augmenting), 155% (inspiratory), 230% (expiratory decrementing), 191% (expiratory augmenting), and 136% (expiratory) of the rates in normoxia. The response to hypoxia was similar in non-rapid-eye-movement (NREM) and REM sleep. Additionally, changes in the profile of activity were observed in all cell types examined. These changes included advanced, prolonged, and abbreviated patterns of activity in response to hypoxia; for example, some inspiratory neurons prolonged their discharge into expiration during the postinspiratory period in hypoxia but not in normoxia. Although changes in activity of the inspiratory neurons could account for the increased breathing efforts and activity of the diaphragm observed during hypoxia, the mechanisms responsible for the change in respiratory rate were not revealed by our data. Address for reprint requests and other correspondence: A. T. Lovering, The John Rankin Laboratory of Pulmonary Medicine, Department of Population Health Sciences, University of Wisconsin Medical School, Room 4245 MSC, 1300 University Ave., Madison, WI 53706-1532 (E-mail: atlovering{at}wisc.edu )
ISSN:0022-3077
1522-1598
DOI:10.1152/jn.00615.2005