1. Activation of the vestibular system produces reflex modulation of expiratory muscle activity. The purpose of the present study was to investigate the possible role of bulbospinal expiratory (E) neurons located in the caudal ventral respiratory group (VRG) in mediating vestibulo-respiratory reflexes. Experiments were carried out in decerebrated, paralyzed, and artificially ventilated cats. 2. Electrical stimulation of the vestibular nerve (VN), using short trains of current pulses, elicited bilateral reflex responses on abdominal muscle nerves (ABDNs). This response was not affected by lesions of the cochlear nuclei made by kainic acid injections. The ABDN response typically consisted of a combination of short-latency excitation and long-latency inhibition on the ipsilateral side and, in contrast, a combination of short-latency inhibition and long-latency excitation on the contralateral side. 3. Extracellular recordings were made from 43 caudal VRG bulbospinal E neurons that were activated antidromically from the contralateral upper lumbar spinal cord. More than 80% of these neurons responded to either ipsi- and/or contralateral VN stimulation. The neuronal response consisted of either a combination of excitation and inhibition or only inhibition. The majority of neurons had response patterns appropriate to contribute to the response observed on the contralateral ABDN; however, the latency of the VRG E neuron response was too long to initiate the ABDN response. 4. To further evaluate the contribution of caudal VRG E neurons to the vestibulo-abdominal reflex, ABDN responses were compared before and after sectioning the axons of caudal VRG bulbospinal E neurons where they cross the midline between the obex and first cervical spinal segment. These midsagittal lesions abolished expiratory modulation of ABDN discharge. The lesions also decreased the amplitude of the vestibular-evoked ABDN response but could not abolish the response. The postlesion amplitude was decreased on average to approximately 70% of prelesion values. 5. In conclusion, although the present results indicate that the majority of caudal VRG bulbospinal E neurons respond appropriately to contribute to the vestibulo-abdominal reflex, the reflex largely is unaffected by the removal of caudal VRG E input. The additional descending inputs that are important for mediating the reflex remain to be investigated and may include vestibulospinal and/or reticulospinal tracts.
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http://dx.doi.org/10.1152/jn.1996.76.4.2271 | DOI Listing |
J Neurophysiol
January 2012
Department of Molecular Pharmacology and Physiology, College of Medicine, University of South Florida, Tampa, Florida 33612-4799, USA.
Ventrolateral respiratory column (VRC) circuits that modulate breathing in response to changes in central chemoreceptor drive are incompletely understood. We employed multielectrode arrays and spike train correlation methods to test predictions of the hypothesis that pre-Bötzinger complex (pre-BötC) and retrotrapezoid nucleus/parafacial (RTN-pF) circuits cooperate in chemoreceptor-evoked tuning of ventral respiratory group (VRG) inspiratory neurons. Central chemoreceptors were selectively stimulated by injections of CO(2)-saturated saline into the vertebral artery in seven decerebrate, vagotomized, neuromuscularly blocked, and artificially ventilated cats.
View Article and Find Full Text PDFJ Neurophysiol
June 2011
Department of Molecular Pharmacology and Physiology and Neuroscience Program, School of Biomedical Sciences, University of South Florida College of Medicine, Tampa, Florida 33612-4799, USA.
The medullary ventral respiratory column (VRC) of neurons is essential for respiratory motor pattern generation; however, the functional connections among these cells are not well understood. A rostral extension of the VRC, including the retrotrapezoid nucleus/parafacial region (RTN-pF), contains neurons responsive to local perturbations of CO(2)/pH. We addressed the hypothesis that both local RTN-pF interactions and functional connections from more caudal VRC compartments--extending from the Bötzinger and pre-Bötzinger complexes to the ventral respiratory group (Böt-VRG)--influence the respiratory modulation of RTN-pF neurons and their responses to central chemoreceptor and baroreflex activation.
View Article and Find Full Text PDFRespir Physiol Neurobiol
August 2010
Department of Pathophysiology, Jessenius Faculty of Medicine in Martin, Commenius University in Bratislava, Sklabinska Str. 26, 036 01 Martin, Slovak Republic.
Central neuronal interaction seems to play a role in pathogenesis of upper airway cough syndrome. In the guinea pig model we used the method c-fos expression to identify neurons involved in processing of nociceptive nasal stimuli and their contribution to enhancement of cough. 21 spontaneously breathing, urethane anaesthetized animals were used.
View Article and Find Full Text PDFProg Brain Res
July 2008
Department of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, PA 19129, USA.
The brainstem respiratory network can operate in multiple functional states engaging different state-dependent neural mechanisms. These mechanisms were studied in the in situ perfused rat brainstem-spinal cord preparation using sequential brainstem transections and administration of riluzole, a pharmacological blocker of persistent sodium current (INaP). Dramatic transformations in the rhythmogenic mechanisms and respiratory motor pattern were observed after removal of the pons and subsequent medullary transactions down to the rostral end of pre-Bötzinger complex (pre-BötC).
View Article and Find Full Text PDFJ Neurosci
October 2003
Department of Neurobiology, Tokyo Metropolitan Institute for Neuroscience, Tokyo 183-8526, Japan.
The medullary respiratory network involves various types of respiratory neurons. The present study focused on possible inhibitory neurons called decrementing expiratory (E-DEC) neurons and aimed to determine whether their transmitter is glycine or GABA. In Nembutal-anesthetized, neuromuscularly blocked, and artificially ventilated rats we labeled E-DEC neurons with Neurobiotin and processed the tissues for detection of mRNA encoding either glycine transporter 2 (GLYT2) as a marker for glycinergic neurons or glutamic acid decarboxylase isoform 67 (GAD67) as a marker for GABAergic neurons, using in situ hybridization.
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