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.

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.

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.

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.

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.

scholarly journals 2019 Ludwig Lecture: Rhythms in sympathetic nerve activity are a key to understanding neural control of the cardiovascular system

2020 ◽  
Vol 318 (2) ◽  
pp. R191-R205 ◽  
Author(s):  
Susan M. Barman
Keyword(s):  
Brain Stem ◽  
Cardiovascular System ◽  
Sympathetic Nerve ◽  
Neural Control ◽  
Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Sympathetic Nerves ◽  
Ventrolateral Medulla ◽  
Nerve Activity

This review is based on the Carl Ludwig Distinguished Lecture, presented at the 2019 Experimental Biology Meeting in Orlando, FL, and provides a snapshot of >40 years of work done in collaboration with the late Gerard L. Gebber and colleagues to highlight the importance of considering the rhythmic properties of sympathetic nerve activity (SNA) and brain stem neurons when studying the neural control of autonomic regulation. After first providing some basic information about rhythms, I describe the patterns and potential functions of rhythmic activity recorded from sympathetic nerves under various physiological conditions. I review the evidence that these rhythms reflect the properties of central sympathetic neural networks that include neurons in the caudal medullary raphe, caudal ventrolateral medulla, caudal ventrolateral pons, medullary lateral tegmental field, rostral dorsolateral pons, and rostral ventrolateral medulla. The role of these brain stem areas in mediating steady-state and reflex-induced changes in SNA and blood pressure is discussed. Despite the common appearance of rhythms in SNA, these oscillatory characteristics are often ignored; instead, it is common to simply quantify changes in the amount of SNA to make conclusions about the function of the sympathetic nervous system in mediating responses to a variety of stimuli. This review summarizes work that highlights the need to include an assessment of the changes in the frequency components of SNA in evaluating the cardiovascular responses to various manipulations as well as in determining the role of different brain regions in the neural control of the cardiovascular system.

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.

Changes in antidromic latencies of medullary respiratory neurons in hypercapnia and hypoxia

1985 ◽  
Vol 59 (4) ◽  
pp. 1208-1213 ◽  
Author(s):  
A. L. Bianchi ◽  
W. M. St John
Keyword(s):  
Membrane Potential ◽  
Neuronal Activity ◽  
Membrane Potentials ◽  
Respiratory Neurons ◽  
Strongly Correlated ◽  
Antidromic Activation ◽  
Axonal Projections ◽  
Medullary Respiratory Neurons ◽  
Spontaneous Neuronal Activity ◽  
The Difference

We evaluated mechanisms underlying changes in discharge frequencies of medullary respiratory neurons. This evaluation was made by determining variations in antidromic latencies; these variations reflect changes in membrane potentials. In decerebrate, vagotomized, paralyzed, and ventilated cats, activities of the phrenic nerve and single respiratory neurons were monitored in hyperoxic normocapnia, hyperoxic hypercapnia, and/or normocapnic hypoxia. Axonal projections were defined as bulbospinal or laryngeal by antidromic activation. At normocapnic hyperoxia, antidromic latencies fell to minima during periods of spontaneous neuronal activity, with maxima occurring between neuronal bursts. In hypercapnia or hypoxia, these minima were not altered, whereas maximum latencies typically rose for neurons whose discharge frequencies increased. However, the increased frequencies most strongly correlated with increases in the difference between maximum and minimum latencies. No such correlation was evident for neurons whose discharge frequencies declined. We conclude that the overall change of membrane potential primarily defines neuronal discharge frequencies. Changes in membrane potentials induced by peripheral and central chemoreceptor afferents and by direct actions of hypercapnia and hypoxia are discussed.

Control of abdominal muscles by brain stem respiratory neurons in the cat

1985 ◽  
Vol 54 (1) ◽  
pp. 155-167 ◽  
Author(s):  
A. D. Miller ◽  
K. Ezure ◽  
I. Suzuki
Keyword(s):  
Brain Stem ◽  
Respiratory Neurons ◽  
Abdominal Muscles ◽  
Antidromic Activation ◽  
Ventral Respiratory Group ◽  
Large Projection ◽  
Retrofacial Nucleus ◽  
Almost All ◽  
L1 And L2 ◽  
Lumbar Cord

Control of abdominal musculature by brain stem respiratory neurons was studied in decerebrate unanesthetized cats by determining 1) which brain stem respiratory neurons could be antidromically activated from the lumbar cord, from which the abdominal muscles receive part of their innervation, and 2) if lumbar-projecting respiratory neurons make monosynaptic connections with abdominal motoneurons. A total of 462 respiratory neurons, located between caudal C2 and the retrofacial nucleus (Botzinger complex), were tested for antidromic activation from the upper lumbar cord. Fifty-eight percent of expiratory (E) neurons (70/121) in the caudal ventral respiratory group (VRG) between the obex and rostral C1 were antidromically activated from contralateral L1. Eight of these neurons were activated at low thresholds from lamina VIII and IX in the L1-2 gray matter. One-third (14/41) of the E neurons that projected to L1 could also be activated from L4-5. Almost all antidromic E neurons had an augmenting firing pattern. Ten scattered inspiratory (I) neurons projected to L1 but could not be activated from L4-5. No neurons that fired during both E and I phases (phase-spanning neurons) were antidromically activated from the lumbar cord. In order to test for possible monosynaptic connections between descending E neurons and abdominal motoneurons, cross-correlations were obtained between 27 VRG E neurons, which were antidromically activated from caudal L2 and contralateral L1 and L2 abdominal nerve activity (47 neuron-nerve combinations). Only two neurons showed a correlation with one of the two nerves tested. Although there is a large projection to the lumbar cord from expiratory neurons in the ventral respiratory group caudal to the obex, cross-correlation analyses suggest that strong monosynaptic connections between these neurons and abdominal motoneurons are scarce.

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