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.

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.

A characterization of the respiratory pattern of gasping

1981 ◽  
Vol 50 (5) ◽  
pp. 984-993 ◽  
Author(s):  
W. M. St John ◽  
K. V. Knuth
Keyword(s):  
Brain Stem ◽  
Phrenic Nerve ◽  
Sodium Cyanide ◽  
Respiratory Pattern ◽  
Nerve Activity ◽  
Ventilatory Pattern ◽  
Brain Stem Lesions ◽  
Stem Lesions ◽  
Pontomedullary Junction

The purpose of this investigation was to compare the respiratory pattern of gasping with eupnea and apneusis. Decerebrate, cerebellectomized, vagotomized, paralyzed and ventilated cats were used. The ventilatory pattern, assessed by phrenic nerve activity, was reversibly altered from eupnea to apneusis or gasping by use of a cooling-for, thermode positioned inm the rostral pons or through the pontomedullary junction, respectively. Irreversible apneusis or gasping resulted from brain stem lesions or freezing at appropriate loci. Analysis of phrenic activity revealed that the rates of onset and rise of the gasp were much greater than those of the eupneic or apneustic inspiration. Moreover, in contrast to eupnea or apneusis, neither the frequency nor the intensity of gasps was altered by hypercapnia, hypocapnia, or carotid chemoreceptor stimulation by sodium cyanide. Although hypoxia caused an increase in gasping frequency, this response was transient and not dependent on carotid chemoreceptor mechanisms. These results provide no support for the concept that common mechanisms localized in medulla, underlie the neurogenesis of all automatic ventilatory patterns.

Respiratory modulation of sympathetic nerve activity: effect of MK-801

1996 ◽  
Vol 270 (3) ◽  
pp. R645-R651 ◽  
Author(s):  
S. F. Morrison
Keyword(s):  
Brain Stem ◽  
Phrenic Nerve ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Respiratory Cycle ◽  
Respiratory Neurons ◽  
Nerve Activity ◽  
Mk 801 ◽  
Nmda Channel ◽  
The Brain

The modulation of splanchnic sympathetic nerve activity (SNA) by brain stem neural networks generating the respiratory rhythm was examined in decerebrate, unanesthetized, vagotomized, artificially ventilated rats before and after blockade of the N-methyl-D-aspartate (NMDA) channel with intravenous administration of dizocilpine (MK-801). NMDA channel blockade 1) prolonged inspiration and reduced the phrenic nerve amplitude, 2) reduced SNA to 40% of control levels, and 3) decreased mean arterial pressure by 20 mmHg. A strong synchronization of SNA to the central respiratory cycle (monitored by the activity on the phrenic nerve) was maintained after MK-801 administration, although a brief inhibition of SNA during early inspiration and a sympathetic excitation during early expiration were eliminated. These results suggest 1) the existence of an NMDA-independent mechanism by which some elements of the brain stem respiratory network excite sympathetic outflow, 2) that the NMDA-mediated influence of specific classes of brain stem respiratory neurons can modulate this excitation during portions of the respiratory cycle, and 3) that an NMDA-dependent excitation in the brain stem or spinal cord plays a significant role in maintaining basal levels of splanchnic SNA.

Arterial pulse modulated activity is expressed in respiratory neural output

2005 ◽  
Vol 99 (2) ◽  
pp. 691-698 ◽  
Author(s):  
Thomas E. Dick ◽  
Roger Shannon ◽  
Bruce G. Lindsey ◽  
Sarah C. Nuding ◽  
Lauren S. Segers ◽  
...  
Keyword(s):  
Brain Stem ◽  
Neural Control ◽  
Respiratory Neurons ◽  
Arterial Pulse ◽  
Pulse Modulation ◽  
Nerve Activity ◽  
Data Set ◽  
Antidromic Activation ◽  
Axonal Projections ◽  
Expiratory Neurons

Although it is well-established that sympathetic activity is modulated with respiration, it is unknown whether neural control of respiration is reciprocally influenced by cardiovascular function. Even though previous studies have suggested the existence of pulse modulation in respiratory neurons, they could not exclude the possibility that such cells were involved in cardiovascular rather than respiratory motor control, owing to neuroanatomic and functional overlaps between brain stem neurons involved in respiratory and cardiovascular control. The aim of this study was to test the hypothesis that respiratory motoneurons and putative premotoneurons are modulated by arterial pulse. An existing data set composed of 72 well-characterized, respiratory-modulated brain stem motoneurons and putative premotoneurons was analyzed using δ2, a recently described statistic that quantifies the magnitude of arterial pulse-modulated spike activity [Dick TE and Morris KF. J Physiol 556: 959–970, 2004]. Neuronal activity was recorded in the rostral and caudal ventral respiratory groups of 19 decerebrate, neuromuscular-blocked, ventilated cats. Axonal projections were identified by rectified and unrectified spike-triggered averages of recurrent laryngeal nerve activity or by antidromic activation from spinal stimulation electrodes. The firing rates of ∼30% of these neurons were modulated in phase with both the respiratory and cardiac cycles. Furthermore, arterial pulse modulation occurred preferentially in the expiratory phase in that only expiratory neurons had high δ2 values and only expiratory activity had significant δ2 values after partitioning tonic activity into the inspiratory and expiratory phases. The results demonstrate that both respiratory motoneurons and putative premotoneuronal activity can be pulse modulated. We conclude that a cardiac cycle-related modulation is expressed in respiratory motor activity, complementing the long-recognized respiratory modulation of sympathetic nerve activity.

Effects of Sevoflurane on Excitatory Neurotransmission to Medullary Expiratory Neurons and on Phrenic Nerve Activity in a Decerebrate Dog Model

2001 ◽  
Vol 95 (2) ◽  
pp. 485-491 ◽  
Author(s):  
Astrid G. Stucke ◽  
Eckehard A. E. Stuth ◽  
Viseslav Tonkovic-Capin ◽  
Mislav Tonkovic-Capin ◽  
Francis A. Hopp ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Phrenic Nerve ◽  
Minimum Alveolar Concentration ◽  
Neuronal Response ◽  
Gamma Aminobutyric Acid ◽  
Nerve Activity ◽  
Gaba A ◽  
Phrenic Nerve Activity ◽  
Synaptic Neurotransmission ◽  
Expiratory Neurons

Background Sevoflurane is a new volatile anesthetic with a pronounced respiratory depressant effect. Synaptic neurotransmission in canine expiratory bulbospinal neurons is mainly mediated by excitatory N-methyl-D-aspartatic acid (NMDA) receptor input and modulated by inhibitory gamma-aminobutyric acid type A (GABA(A)) receptors. The authors investigated the effect of sevoflurane on these mechanisms in decerebrate dogs. Methods Studies were performed in decerebrate, vagotomized, paralyzed and mechanically ventilated dogs during hypercapnic hyperoxia. The effect of 1 minimum alveolar concentration (MAC; 2.4%) sevoflurane on extracellularly recorded neuronal activity was measured during localized picoejection of the glutamate agonist NMDA and the GABA(A) receptor blocker bicuculline in a two-part protocol. First, complete blockade of the GABA(A)ergic mechanism by bicuculline allowed differentiation between the effects of sevoflurane on overall GABA(A)ergic inhibition and on overall glutamatergic excitation. In a second step, the neuronal response to exogenous NMDA was used to estimate sevoflurane's effect on postsynaptic glutamatergic neurotransmission. Results One minimum alveolar concentration sevoflurane depressed the spontaneous activity of 16 expiratory neurons by 36.7+/-22.4% (mean +/- SD). Overall glutamatergic excitation was depressed 19.5+/-16.2%, and GABA(A)ergic inhibition was enhanced 18.7+/-20.6%. However, the postsynaptic response to exogenous NMDA was not significantly altered. In addition, 1 MAC sevoflurane depressed peak phrenic nerve activity by 61.8+/-17.7%. Conclusions In the authors' in vivo expiratory neuronal model, the depressive effect of sevoflurane on synaptic neurotransmission was caused by a reduction of presynaptic glutamatergic excitation and an enhancement of GABA(A)ergic inhibition. The effects on expiratory neuronal activity were similar to halothane, but sevoflurane caused a stronger depression of phrenic nerve activity than halothane.

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.

Medullary respiratory neuron activity: relationship to tonic and phasic REM sleep

1980 ◽  
Vol 48 (1) ◽  
pp. 54-65 ◽  
Author(s):  
J. Orem
Keyword(s):  
Brain Stem ◽  
Rem Sleep ◽  
Respiratory Activity ◽  
Regression Line ◽  
Respiratory Neurons ◽  
Neuron Activity ◽  
Respiratory Neuron ◽  
Dorsal Respiratory Group ◽  
Phasic Rem Sleep ◽  
The Relationship

This study analyzes the relationship of brain stem respiratory neuron activity to the tonic and phasic events of rapid-eye-movement (REM) sleep. Dorsal and ventral medullary respiratory neurons were recorded in sleeping cats. Discharges of inspiratory and expiratory cells increased in number and frequency with increases in pontogeniculooccipital (PGO) spiking (phasic REM activity). Across neurons the correlations between PGO wave frequency and respiratory neuron activity were positively related to the discharge levels of the neurons: the more active the cell, the greater the relationship to PGO activity. Tonic REM influences on respiratory neurons were calculated by extrapolating from the regression line relating PGO frequency and neuron activity to the hypothetical state of no PGO activity. These calculated levels, when compared to non-REM sleep levels, showed that tonic REM mechanisms reduced the activity of some neurons and activated others. Ventral medullary respiratory activity generally was decreased during tonic rem, whereas dorsal respiratory group cells were variously activated and inactivated. These results demonstrate an association of brain stem respiratory activity to nonrespiratory REM sleep variables.

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