Responses of two or more respiratory neurons to stimulation of inspiratory and expiratory zones of the gigantocellular nucleus

1983 ◽  
Vol 95 (1) ◽  
pp. 15-17
Author(s):  
M. V. Sergievskii ◽  
N. Ya. Kireeva
Keyword(s):  
Respiratory Neurons ◽  
Gigantocellular Nucleus ◽  
Stimulation Of

Fastigial nucleus-mediated respiratory responses depend on the medullary gigantocellular nucleus

2001 ◽  
Vol 91 (4) ◽  
pp. 1713-1722 ◽  
Author(s):  
Fadi Xu ◽  
Tongrong Zhou ◽  
Tonya Gibson ◽  
Donald T. Frazier
Keyword(s):  
Electrical Stimulation ◽  
Ibotenic Acid ◽  
Major Effect ◽  
Fastigial Nucleus ◽  
Respiratory Response ◽  
The Right ◽  
Spontaneously Breathing ◽  
Respiratory Responses ◽  
Gigantocellular Nucleus ◽  
Stimulation Of

Electrical stimulation of the rostral fastigial nucleus (FNr) alters respiration via activation of local neurons. We hypothesized that this FNr-mediated respiratory response was dependent on the integrity of the nucleus gigantocellularis of the medulla (NGC). Electrical stimulation of the FNr in 15 anesthetized and tracheotomized spontaneously breathing rats significantly altered ventilation by 35.2 ± 11.0% ( P < 0.01) with the major effect being excitatory (78%). This respiratory response did not significantly differ from control after lesions of the NGC via bilateral microinjection of kainic or ibotenic acid (4.5 ± 1.9%; P > 0.05) but persisted in sham controls. Eight other rats, in which horseradish peroxidase (HRP) solution was previously microinjected into the left NGC, served as nonstimulation controls or were exposed to either 15-min repeated electrical stimulation of the right FNr or hypercapnia for 90 min. Histochemical and immunocytochemical data showed that the right FNr contained clustered HRP-labeled neurons, most of which were double labeled with c-Fos immunoreactivity in both electrically and CO2-stimulated rats. We conclude that the NGC receives monosynaptic FNr inputs and is required for fully expressing FNr-mediated respiratory responses.

scholarly journals Blood pressure changes alter tracheobronchial cough: computational model of the respiratory-cough network and in vivo experiments in anesthetized cats

2011 ◽  
Vol 111 (3) ◽  
pp. 861-873 ◽  
Author(s):  
Ivan Poliacek ◽  
Kendall F. Morris ◽  
Bruce G. Lindsey ◽  
Lauren S. Segers ◽  
Melanie J. Rose ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Motor Pattern ◽  
Esophageal Pressure ◽  
Respiratory Neurons ◽  
Cycle Duration ◽  
In Vivo Experiments ◽  
Arterial Blood ◽  
Posterior Cricoarytenoid ◽  
Stimulation Of

We tested the hypothesis, motivated in part by a coordinated computational cough network model, that alterations of mean systemic arterial blood pressure (BP) influence the excitability and motor pattern of cough. Model simulations predicted suppression of coughing by stimulation of arterial baroreceptors. In vivo experiments were conducted on anesthetized spontaneously breathing cats. Cough was elicited by mechanical stimulation of the intrathoracic airways. Electromyograms (EMG) of inspiratory parasternal, expiratory abdominal, laryngeal posterior cricoarytenoid (PCA), and thyroarytenoid muscles along with esophageal pressure (EP) and BP were recorded. Transiently elevated BP significantly reduced cough number, cough-related inspiratory, and expiratory amplitudes of EP, peak parasternal and abdominal EMG, and maximum of PCA EMG during the expulsive phase of cough, and prolonged the cough inspiratory and expiratory phases as well as cough cycle duration compared with control coughs. Latencies from the beginning of stimulation to the onset of cough-related diaphragm and abdominal activities were increased. Increases in BP also elicited bradycardia and isocapnic bradypnea. Reductions in BP increased cough number; elevated inspiratory EP amplitude and parasternal, abdominal, and inspiratory PCA EMG amplitudes; decreased total cough cycle duration; shortened the durations of the cough expiratory phase and cough-related abdominal discharge; and shortened cough latency compared with control coughs. Reduced BP also produced tachycardia, tachypnea, and hypocapnic hyperventilation. These effects of BP on coughing likely originate from interactions between barosensitive and respiratory brainstem neuronal networks, particularly by modulation of respiratory neurons within multiple respiration/cough-related brainstem areas by baroreceptor input.

Neural mechanisms of sneeze

1975 ◽  
Vol 229 (3) ◽  
pp. 770-776 ◽  
Author(s):  
HL Batsel ◽  
AJ Lines
Keyword(s):  
High Frequency ◽  
Neural Mechanisms ◽  
Nucleus Ambiguus ◽  
Respiratory Neurons ◽  
Similar Response ◽  
Response Patterns ◽  
Nerve Activity ◽  
Inspiratory Neurons ◽  
Expiratory Neurons ◽  
Stimulation Of

Sneezes were induced in anestized cats by repetitive stimulation of the ethmoidal nerve. Activity of bulbar respiratory neurons during sneezing was recorded extracellularly through tungsten microelectrodes. Most expiratory neurons could be locked onto the stimulus pulses so that they responded either throughout inspiration as well as expiration or so that they began responding at some time during inspiration. As inspiration approached termination, multiple spiking occurred, finally to result in high-frequency bursts which just preceded active expiration. A fraction of expiratory neurons were activated only in bursts. Latent expiratory neurons were recruited in sneezing. Inspiratory neurons near nucleus ambiguus and most of those near fasciculus solitarius displayed similar response patterns consisting of silent periods followed by delayed smooth activations. Temporal characteristics of the silent periods, "inhibitory gaps," suggested that they resulted from inhibition whose source was the expiratory neurons which were driven throughout inspriation. Some inspiratory neurons in the area of fasciculus solitarius failed to exhibit inhibitory gaps.

Responses of Respiratory Neurons in the Medulla Oblongata to Stimulation of the Septal Nuclei during Hypoxia

2004 ◽  
Vol 34 (1) ◽  
pp. 105-108 ◽  
Author(s):  
N. S. Akopyan ◽  
N. Yu. Adamyan ◽  
N. V. Sarkisyan ◽  
R. S. Arutyunyan
Keyword(s):  
Medulla Oblongata ◽  
Respiratory Neurons ◽  
Septal Nuclei ◽  
Stimulation Of

Midbrain and medullary control of postinspiratory activity of the crural and costal diaphragm in vivo

2011 ◽  
Vol 105 (6) ◽  
pp. 2852-2862 ◽  
Author(s):  
Hari H. Subramanian ◽  
Gert Holstege
Keyword(s):  
Inhibitory Effect ◽  
Respiratory Neurons ◽  
Abdominal Muscles ◽  
Anesthetized Rats ◽  
Diaphragm Function ◽  
Three Phase ◽  
Crural Diaphragm ◽  
Decerebrate Cats ◽  
Stimulation Of

Studies on brain stem respiratory neurons suggest that eupnea consists of three phases: inspiration, postinspiration, and expiration. However, it is not well understood how postinspiration is organized in the diaphragm, i.e., whether postinspiration differs in the crural and costal segments of the diaphragm and what the influence is of postinspiratory neurons on diaphragm function during eupnea. In this in vivo study we investigated the postinspiratory activity of the two diaphragm segments during eupnea and the changes in diaphragm function following modulation of eupnea. Postinspiratory neurons in the medulla were stereotaxically localized extracellularly and neurochemically stimulated. We used three types of preparations: precollicularly decerebrated unanesthetized cats and rats and anesthetized rats. In all preparations, during eupnea, postinspiratory activity was found in the crural but not in the costal diaphragm. When eupnea was discontinued in decerebrate cats in which stimulation in the nucleus retroambiguus induced activation of laryngeal or abdominal muscles, all postinspiratory activity in the crural diaphragm was abolished. In decerebrate rats, stimulation of the midbrain periaqueductal gray abolished postinspiration in the crural diaphragm but induced activation in the costal diaphragm. In anesthetized rats, stimulation of medullary postinspiratory neurons abolished the postinspiratory activity of the crural diaphragm. Vagal nerve stimulation in these rats increased the intensity of postinspiratory neuronal discharge in the solitary nucleus, leading to decreased activity of the crural diaphragm. These data demonstrate that three-phase breathing in the crural diaphragm during eupnea exists in vivo and that postinspiratory neurons have an inhibitory effect on crural diaphragm function.

Muscle afferents and activity of respiratory neurons

1961 ◽  
Vol 200 (4) ◽  
pp. 679-684 ◽  
Author(s):  
K. Koizumi ◽  
J. Ushiyama ◽  
C. McC. Brooks
Keyword(s):  
Muscle Afferents ◽  
Monosynaptic Reflex ◽  
Respiratory Neurons ◽  
Group I ◽  
Afferent Fibers ◽  
Intercostal Nerves ◽  
Polysynaptic Reflexes ◽  
Root Stimulation ◽  
Mixed Nerve ◽  
Stimulation Of

Respiratory effects of stimulating afferent fibers of muscle, skin and mixed nerve were determined in Nembutal-anesthetized cats. Repetitive stimuli which produced only monosynaptic reflex actions caused augmentation of respiration. When stronger stimuli also activated fibers of a smaller diameter than group I afferents, polysynaptic reflexes were evoked and greater changes in respiration resulted. Volume rather than rate changes were induced by stimulation of these muscle afferents. Microelectrodes were used to record from respiratory neurons of the medulla and pons. Most neurons fired in conjunction with inspiration; stimulation of muscle afferents advanced time of firing and increased frequency of discharge. Neurons firing in conjunction with expiration were inhibited by muscle afferents. A few neurons of the pons showed respiration-linked activity modified by afferent nerve stimulation. Segmental reflex discharges, out intercostal nerves, elicited by dorsal root stimulation were found to be inhibited by stimulation of muscle afferents. Discharges from muscle receptors affect ventilatory volumes and activities of medullary neurons which seemingly participate in the control of respiration.

Response of Laryngeal Airway Resistance to Chemoreceptor Stimulation: Effect of Pulmonary Afferent Denervation

1982 ◽  
Vol 90 (6) ◽  
pp. 723-727
Author(s):  
Thomas V. McCaffrey
Keyword(s):  
Airway Resistance ◽  
Afferent Input ◽  
Respiratory Neurons ◽  
Vagus Nerves ◽  
Before And After ◽  
Bilateral Vagotomy ◽  
Recurrent Laryngeal Nerves ◽  
Laryngeal Resistance ◽  
Stimulation Of ◽  
Laryngeal Airway

The response of laryngeal airway resistance to chemoreceptor stimulation was measured before and after vagotomy in ten anesthetized dogs. With the vagus nerves intact, stimulation of chemoreceptors produced a decrease in both inspiratory and expiratory laryngeal resistance. After bilateral vagotomy below the origin of the recurrent laryngeal nerves, stimulation of chemoreceptors produced a smaller decrease in inspiratory laryngeal resistance and an increase in expiratory laryngeal resistance. We concluded that pulmonary afferent input to the respiratory neurons maintains a low airway resistance during chemoreceptor stimulation.

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