Differing activities of medullary respiratory neurons in eupnea and gasping

1991 ◽  
Vol 70 (3) ◽  
pp. 1265-1270 ◽  
Author(s):  
D. Zhou ◽  
M. J. Wasicko ◽  
J. M. Hu ◽  
W. M. St John
Keyword(s):  
Carbon Monoxide ◽  
Brain Stem ◽  
Phrenic Nerve ◽  
Peak Discharge ◽  
Discharge Frequency ◽  
Respiratory Neurons ◽  
Ventilatory Pattern ◽  
Medullary Respiratory Neurons ◽  
Inspiratory Neurons ◽  
Expiratory Neurons

Our purpose was to compare further eupneic ventilatory activity with that of gasping. Decerebrate, paralyzed, and ventilated cats were used; the vagi were sectioned within the thorax caudal to the laryngeal branches. Activities of the phrenic nerve and medullary respiratory neurons were recorded. Antidromic invasion was used to define bulbospinal, laryngeal, or not antidromically activated units. The ventilatory pattern was reversibly altered to gasping by exposure to 1% carbon monoxide in air. In eupnea, activities of inspiratory neurons commenced at various times during inspiration, and for most the discharge frequency gradually increased. In gasping, the peak discharge frequency of inspiratory neurons was unaltered. However, all commenced activities at the start of the phrenic burst and reached peak discharge almost immediately. The discharge frequencies of all groups of expiratory neurons fell in gasping, with many neurons ceasing activity entirely. These data are consistent with the hypothesis that brain stem mechanisms controlling eupnea and gasping differ fundamentally.

Respiratory neuron responses to hypercapnia and carotid chemoreceptor stimulation

1981 ◽  
Vol 51 (4) ◽  
pp. 816-822 ◽  
Author(s):  
W. M. St John
Keyword(s):  
Brain Stem ◽  
Reticular Formation ◽  
Phrenic Nerve ◽  
Sodium Cyanide ◽  
Respiratory Neurons ◽  
Respiratory Neuron ◽  
Nerve Activity ◽  
Dorsal Nucleus ◽  
Central Chemoreceptors ◽  
Expiratory Neurons

In decerebrate, vagotomized, paralyzed, and ventilated cats, activities were recorded from the phrenic nerve and from respiratory units within the dorsal and ventral medullary respiratory nuclei and the pontile reticular formation. These unit activities were monitored during equivalent augmentations in peak integrated phrenic nerve activity induced by stimuli acting primarily on the peripheral or central chemoreceptors. These stimuli were intracarotid infusions of sodium cyanide or nicotine and exposure to hyperoxic hypercapnia, respectively. Both stimuli caused similar increases in activities for most dorsal nucleus inspiratory units. For units of the ventral medullary nucleus, augmentations in activity were only significant (inspiratory neurons) or were of greater magnitude (expiratory neurons) during hypercapnia. As opposed to medullary units, the discharge frequencies of many pontile units were unaltered or declined during both peripheral and central chemoreceptor stimulations. These results support the concept that excitatory influences from the peripheral and central chemoreceptors are not equally distributed among all groups of brain stem respiratory neurons.

scholarly journals Opioid Receptors on Bulbospinal Respiratory Neurons Are Not Activated During Neuronal Depression by Clinically Relevant Opioid Concentrations

2008 ◽  
Vol 100 (5) ◽  
pp. 2878-2888 ◽  
Author(s):  
Astrid G. Stucke ◽  
Edward J. Zuperku ◽  
Antonio Sanchez ◽  
Mislav Tonkovic-Capin ◽  
Viseslav Tonkovic-Capin ◽  
...  
Keyword(s):  
Receptor Agonist ◽  
Network Effects ◽  
Peak Discharge ◽  
Discharge Frequency ◽  
Respiratory Neurons ◽  
Premotor Neurons ◽  
Significant Depression ◽  
Expiratory Neurons ◽  
Opioid Receptor Agonists ◽  
Deltorphin Ii

Opioids depress the activity of brain stem respiratory-related neurons, but it is not resolved whether the mechanism at clinical concentrations consists of direct neuronal effects or network effects. We performed extracellular recordings of discharge activity of single respiratory neurons in the caudal ventral respiratory group of decerebrate dogs, which were premotor neurons with a likelihood of 90%. We used multibarrel glass microelectrodes, which allowed concomitant highly localized picoejection of opioid receptor agonists or antagonists onto the neuron. Picoejection of the μ receptor agonist [d-Ala2, N-Me-phe4, gly-ol5]-enkephalin (DAMGO, 1 mM) decreased the peak discharge frequency (mean ± SD) of expiratory neurons to 68 ± 22% ( n = 12), the δ1 agonist d-Pen2,5-enkephalin (DPDPE, 1 mM) to 95 ± 11% ( n = 15), and δ2 receptor agonist [d-Ala2] deltorphin-II to 86 ± 17% (1 mM, n = 15). The corresponding values for inspiratory neurons were: 64 ± 12% ( n = 11), 48 ± 30% ( n = 12), and 75 ± 15% ( n = 11), respectively. Naloxone fully reversed these effects. Picoejection of morphine (0.01–1 mM) depressed most neurons in a concentration dependent fashion to maximally 63% ( n = 27). Picoejection of remifentanil (240–480 nM) did not cause any significant depression of inspiratory ( n = 11) or expiratory neurons ( n = 9). 4. Intravenous remifentanil (0.2–0.6 μg·kg−1·min−1) decreased neuronal peak discharge frequency to 60 ± 12% (inspiratory, n = 7) and 58 ± 11% (expiratory, n = 11). However, local picoejection of naloxone did not reverse the neuronal depression. Our data suggest that μ, δ1, and δ2 receptors are present on canine respiratory premotor neurons. Clinical concentrations of morphine and remifentanil caused no local depression. This lack of effect and the inability of local naloxone to reverse the neuronal depression by intravenous remifentanil suggest that clinical concentrations of opioids produce their depressive effects on mechanisms upstream from respiratory bulbospinal premotor neurons.

Functional associations among simultaneously monitored lateral medullary respiratory neurons in the cat. II. Evidence for inhibitory actions of expiratory neurons

1987 ◽  
Vol 57 (4) ◽  
pp. 1101-1117 ◽  
Author(s):  
B. G. Lindsey ◽  
L. S. Segers ◽  
R. Shannon
Keyword(s):  
Discharge Rate ◽  
Respiratory Neurons ◽  
Short Time Scale ◽  
Axonal Projections ◽  
Medullary Respiratory Neurons ◽  
Antidromic Stimulation ◽  
Expiratory Neurons ◽  
Short Time ◽  
And Control ◽  
The Brain

Arrays of extracellular electrodes were used to monitor simultaneously several (2-8) respiratory neurons in the lateral medulla of anesthetized, paralyzed, bilaterally vagotomized, artificially ventilated cats. Efferent phrenic nerve activity was also recorded. The average discharge rate as a function of time in the respiratory cycle was determined for each neuron. Most cells were tested for spinal or vagal axonal projections using antidromic stimulation methods. Cross-correlational methods were used to analyze spike trains of 480 cell pairs. Each pair included at least one neuron most active during the expiratory phase. All simultaneously recorded neurons were located in the same side of the brain stem. Twenty-six percent (33/129) of the expiratory (E) neuron pairs exhibited short time scale correlations indicative of paucisynaptic interactions or shared inputs, whereas 8% (27/351) of the pairs consisting of an E neuron and an inspiratory (I) cell were similarly correlated. Evidence for several inhibitory actions of E neurons was found: 1) inhibition of I neurons by E neurons with both decrementing (DEC) and augmenting (AUG) firing patterns; 2) inhibition of E-DEC and E-AUG neurons by E-DEC cells; 3) inhibition of E-DEC and E-AUG neurons by E-AUG neurons; and 4) inhibition of E-DEC neurons by tonic I-E phase-spanning cells. Because several cells were recorded simultaneously, direct evidence for concurrent parallel and serial inhibitory processes was also obtained. The results suggest and support several hypotheses for mechanisms that may help to generate and control the pattern and coordination of respiratory motoneuron activities.

Responses of bulbospinal and laryngeal respiratory neurons to hypercapnia and hypoxia

1985 ◽  
Vol 59 (4) ◽  
pp. 1201-1207 ◽  
Author(s):  
W. M. St John ◽  
A. L. Bianchi
Keyword(s):  
Spinal Cord ◽  
Recurrent Laryngeal Nerve ◽  
Phrenic Nerve ◽  
Action Potentials ◽  
Respiratory Muscles ◽  
Laryngeal Nerve ◽  
Respiratory Neurons ◽  
Peripheral Chemoreceptor ◽  
Medullary Respiratory Neurons ◽  
Neuronal Groups

The purpose was to evaluate activities of medullary respiratory neurons during equivalent changes in phrenic discharge resulting from hypercapnia and hypoxia. Decerebrate, cerebellectomized, paralyzed, and ventilated cats were used. Vagi were sectioned at left midcervical and right intrathoracic levels caudal to the origin of right recurrent laryngeal nerve. Activities of phrenic nerve and single respiratory neurons were monitored. Neurons exhibiting antidromic action potentials following stimulations of the spinal cord and recurrent laryngeal nerve were designated, respectively, bulbospinal or laryngeal. The remaining neurons were not antidromically activated. Hypercapnia caused significant augmentations of discharge frequencies for all neuronal groups. Many of these neurons had no change or declines of activity in hypoxia. We conclude that central chemoreceptor afferent influences are ubiquitous, but excitatory influences from carotid chemoreceptors are more limited in distribution among medullary respiratory neurons. Hypoxia will increase activities of neurons that receive sufficient excitatory peripheral chemoreceptor afferents to overcome direct depression by brain stem hypoxia. The possibility that responses of respiratory muscles to hypoxia are programmed within the medulla is discussed.

Excitatory connections between upper cervical inspiratory neurons and phrenic motoneurons in cats

1994 ◽  
Vol 77 (2) ◽  
pp. 679-683 ◽  
Author(s):  
Y. Nakazono ◽  
M. Aoki
Keyword(s):  
Phrenic Nerve ◽  
Respiratory Neurons ◽  
Transmission Delays ◽  
Phrenic Motoneurons ◽  
Inspiratory Neurons ◽  
Upper Cervical ◽  
Cervical Segment ◽  
Focal Cooling ◽  
Descending Influences ◽  
Phrenic Motoneuron

This study aimed to determine whether upper cervical inspiratory neurons (UCINs), which are localized in the intermediolateral part of the gray matter of the upper cervical segments, have propriospinal connections to phrenic motoneurons of the ipsilateral lower cervical segment in anesthetized cats. Unit action potentials of UCINs were extracellularly recorded simultaneously with ipsilateral phrenic nerve activity. To eliminate the descending influences from medullary respiratory neurons to phrenic motoneurons, bulbospinal conduction paths were temporarily blocked by focal cooling applied to the ventral caudal medulla at the pyramidal decussation level by means of a cooling thermode (1 mm tip diam). By using a spike-triggered method, during cooling phrenic nerve activities were evoked by UCIN spikes that were elicited by microinjection of L-glutamate for 20 of the 55 (36%) UCIN units examined. The onset latencies of these phrenic motoneuron responses ranged from 1.5 to 7.1 ms (mean 3.6 ms), depending on synaptic transmission delays. These results clearly demonstrate that UCINs have, at least in part, excitatory mono- and paucisynaptic connections with ipsilateral phrenic motoneurons.

The Effects of Nasal Flow Stimulation on Central Respiratory Pattern

1995 ◽  
Vol 9 (4) ◽  
pp. 203-208 ◽  
Author(s):  
Satoshi Nonaka ◽  
Akihiro Katada ◽  
Kizuku Nakajima ◽  
Takashi Ohsaki ◽  
Tokuji Unno
Keyword(s):  
Cycle Time ◽  
Suppressive Effect ◽  
Respiratory Cycle ◽  
Respiratory Pattern ◽  
Respiratory Neurons ◽  
Electromyographic Activity ◽  
Inspiratory Neurons ◽  
Expiratory Neurons ◽  
Flow Stimulation ◽  
Nasal Flow

The purpose of this study was to analyze the functional role of nasal afferents on central respiratory mechanisms. The electromyographic activity of the diaphragm and the neuronal activities of respiratory neurons within the brainstem were recorded during nasal flow stimulation, using decerebrate cats. Flow stimulation delivered to the nose prolonged the respiratory cycle time and decreased the amplitude of diaphragmatic activity. The respiratory cycle time was prolonged due to prolongation of expiratory phase. Cool air flow stimulation was more effective for changing the respiratory pattern than was warm air. All recorded inspiratory neurons of the dorsal respiratory group decreased their firing rate during stimulation, but more than half of expiratory neurons of the ventral respiratory group did not change. These results suggest that nasal afferents which respond to temperature can modulate the central respiratory pattern and have a stronger suppressive effect on the activity of inspiratory neurons than that of expiratory neurons.

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.

GABAergic effects on respiratory neuronal discharge during opossum development

1993 ◽  
Vol 264 (2) ◽  
pp. R331-R336
Author(s):  
J. P. Farber
Keyword(s):  
Gabaa Receptors ◽  
Breathing Pattern ◽  
Age Groups ◽  
Neuronal Firing ◽  
Respiratory Neurons ◽  
Gamma Aminobutyric Acid ◽  
Firing Rates ◽  
Medullary Respiratory Neurons ◽  
Expiratory Neurons ◽  
Gabaa Antagonist

Changes in breathing pattern between immature and adult animals could be due in part to changing postsynaptic sensitivity to particular neurotransmitters by respiratory neurons and/or to the fate of these neurotransmitters after release. To probe for such effects, gamma-aminobutyric acid (GABA) and the GABAA antagonist, bicuculline, were pressure injected by micropipette in very small volumes (approximately 25 pl) near identified medullary respiratory neurons in Inactin-anesthetized adult and suckling opossums. At a concentration of 10 mM, GABA induced suppression of respiratory neurons firing in animals from about 3 wk of age (the youngest animals tested) onward, with the largest responses occurring in adults. For those age groups tested with 0.5 and 50 mM GABA, shorter and longer responses, respectively, were observed. Bicuculline increased the discharge of respiratory units at all ages tested, but responses normalized to initial firing rates did not systematically differ between sucklings down to 4 wk of age and adults. Bicuculline also influenced the onset and cessation of firing in both inspiratory and expiratory neurons. Discharge of respiratory neurons in immature suckling opossums is characterized by few spikes and low firing rates with each breath. However, recovery of neuronal firing from an exogenous load of GABA and release of neuronal firing after antagonism of GABAA receptors does not show a developmental pattern that would implicate GABA as the crucial mediator of these effects.

Respiratory muscle control during vomiting

1990 ◽  
Vol 68 (2) ◽  
pp. 237-241 ◽  
Author(s):  
Alan D. Miller
Keyword(s):  
Response Pattern ◽  
Respiratory Muscles ◽  
Respiratory Neurons ◽  
Abdominal Muscles ◽  
Inspiratory Muscles ◽  
Medullary Respiratory Neurons ◽  
Gastric Contents ◽  
Expiratory Neurons ◽  
Expiratory Muscles ◽  
Thoracic And Abdominal

The changes in thoracic and abdominal pressures that generate vomiting are produced by coordinated action of the major respiratory muscles. During vomiting, the diaphragm and external intercostal (inspiratory) muscles co-contract with abdominal (expiratory) muscles in a series of bursts of activity that culminates in expulsion. Internal intercostal (expiratory) muscles contract out of phase with these muscles during retching and are inactive during expulsion. The periesophageal portion of the diaphragm relaxes during expulsion, presumably facilitating rostral movement of gastric contents. Recent studies have begun to examine to what extent medullary respiratory neurons are involved in the control of these muscles during vomiting. Bulbospinal expiratory neurons in the ventral respiratory group caudal to the obex discharge at the appropriate time during (fictive) vomiting to activate either abdominal or internal intercostal motoneurons. The pathways that drive phrenic and external intercostal motoneurons during vomiting have yet to be identified. Most bulbospinal inspiratory neurons in the dorsal and ventral respiratory groups do not have the appropriate response pattern to initiate activation of these motoneurons during (fictive) vomiting. Relaxation of the periesophageal diaphragm during vomiting could be brought about, at least in part, by reduced firing of bulbospinal inspiratory neurons.Key words: brain stem, bulbospinal respiratory neurons, vomiting center critique, diaphragm, abdominal muscles.

Opiate slowing of feline respiratory rhythm and effects on putative medullary phase-regulating neurons

2006 ◽  
Vol 290 (5) ◽  
pp. R1387-R1396 ◽  
Author(s):  
Peter M. Lalley
Keyword(s):  
Action Potential ◽  
Respiratory Rhythm ◽  
Input Resistance ◽  
Membrane Depolarization ◽  
Respiratory Neurons ◽  
Response Analysis ◽  
Inspiratory Neurons ◽  
Potential Shape ◽  
Expiratory Neurons

Opiates have effects on respiratory neurons that depress tidal volume and air exchange, reduce chest wall compliance, and slow rhythm. The most dose-sensitive opioid effect is slowing of the respiratory rhythm through mechanisms that have not been thoroughly investigated. An in vivo dose-response analysis was performed on medullary respiratory neurons of adult cats to investigate two untested hypotheses related to mechanisms of opioid-mediated rhythm slowing: 1) Opiates suppress intrinsic conductances that limit discharge duration in medullary inspiratory and expiratory neurons, and 2) opiates delay the onset and lengthen the duration of discharges postsynaptically in phase-regulating postinspiratory and late-inspiratory neurons. In anesthetized and unanesthetized decerebrate cats, a threshold dose (3 μg/kg) of the μ-opioid receptor agonist fentanyl slowed respiratory rhythm by prolonging discharges of inspiratory and expiratory bulbospinal neurons. Additional doses (2–4 μg/kg) of fentanyl also lengthened the interburst silent periods in each type of neuron and delayed the rate of membrane depolarization to firing threshold without altering synaptic drive potential amplitude, input resistance, peak action potential frequency, action potential shape, or afterhyperpolarization. Fentanyl also prolonged discharges of postinspiratory and late-inspiratory neurons in doses that slowed the rhythm of inspiratory and expiratory neurons without altering peak membrane depolarization and hyperpolarization, input resistance, or action potential properties. The temporal changes evoked in the tested neurons can explain the slowing of network respiratory rhythm, but the lack of significant, direct opioid-mediated membrane effects suggests that actions emanating from other types of upstream bulbar respiratory neurons account for rhythm slowing.

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