Respiratory-modulated facial (VII) nerve discharge includes pre-inspiratory (Pre-I) and inspiratory (I) components. Tonic VII bursting is also present across the respiratory cycle. We tested the hypothesis that hypoxia-induced plasticity of VII motor activity is differentially expressed in Pre-I, I and tonic bursting. Phrenic and VII neurograms were recorded in urethane-anesthetized, vagotomized and ventilated adult rats. A 3 min isocapnic hypoxic challenge (PaO(2)=33+/-2 mmHg) was used to evoke respiratory short-term potentiation (STP). Pre-I, I and tonic VII activity increased immediately at the initial stage of hypoxia (i.e. acute response) and then progressively increased as hypoxia was maintained. Following hypoxia, I VII activity remained elevated (i.e. post-hypoxia STP) but both Pre-I and tonic activity immediately returned to baseline values. We conclude that STP following hypoxia is preferentially expressed in I compared to Pre-I and tonic VII activity.
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http://dx.doi.org/10.1016/j.resp.2010.06.015 | DOI Listing |
Respir Physiol Neurobiol
August 2014
Division of Anesthesiology, Department of Clinical Care Medicine, Kanagawa Dental College, Yokosuka City, Kanagawa 238-8580, Japan.
Endogenous neuropeptides known as orexins (hypocretins) play important roles in the regulation of feeding, drinking, endocrine function, and sleep/wakefulness. Orexin neuron projection sites include the rostral ventrolateral medulla of brainstem, which is related to the control of breathing. Previous studies suggest that orexins modulate the central CO2 ventilatory response during wakefulness in rodent.
View Article and Find Full Text PDFRespir Physiol Neurobiol
August 2010
University of Florida, College of Public Health and Health Professions, McKnight Brain Institute, Department of Physical Therapy, PO Box 100154, 100 Newell Dr, Gainesville, FL 32610, United States.
Respiratory-modulated facial (VII) nerve discharge includes pre-inspiratory (Pre-I) and inspiratory (I) components. Tonic VII bursting is also present across the respiratory cycle. We tested the hypothesis that hypoxia-induced plasticity of VII motor activity is differentially expressed in Pre-I, I and tonic bursting.
View Article and Find Full Text PDFRespir Physiol Neurobiol
June 2002
Department of Physiology and Biophysics, State University of New York at Stony Brook, Stony Brook, NY 11794-8661, USA.
We have previously demonstrated that chemical stimulation of the pre-Bötzinger complex (pre-BötC) in the anesthetized cat produces either phasic or tonic excitation of phrenic nerve discharge. This region is characterized by a mixture of inspiratory-modulated, expiratory-modulated, and phase-spanning (including pre-inspiratory (pre-I)) neurons; however, its influence on expiratory motor output is unknown. We, therefore, examined the effects of chemical stimulation of the pre-BötC on expiratory motor output recorded from the caudal iliohypogastric (lumbar, L(2)) nerve.
View Article and Find Full Text PDFJ Neurophysiol
July 1999
Cellular and Systems Neurobiology Section, Laboratory of Neural Control, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA.
We have proposed models for the ionic basis of oscillatory bursting of respiratory pacemaker neurons in the pre-Bötzinger complex. In this paper, we investigate the frequency control and synchronization of these model neurons when coupled by excitatory amino-acid-mediated synapses and controlled by convergent synaptic inputs modeled as tonic excitation. Simulations of pairs of identical cells reveal that increasing tonic excitation increases the frequency of synchronous bursting, while increasing the strength of excitatory coupling between the neurons decreases the frequency of synchronous bursting.
View Article and Find Full Text PDFExp Brain Res
April 1998
Department of Physiology, Showa University, School of Medicine, Tokyo, Japan.
We analysed the modulation of respiratory neurons by adrenaline or noradrenaline (NA) in a newborn rat brainstem-spinal cord preparation. Adrenaline or NA caused a dose-dependent depression of the respiratory rhythm and induced C4 spinal tonic discharges. The inhibitory effect of adrenaline (ED50=0.
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