scholarly journals Characterization of respiratory neurons in the rostral ventrolateral medulla, an area critical for vocal production in songbirds

2013 ◽  
Vol 109 (4) ◽  
pp. 948-957 ◽  
Author(s):  
Judith McLean ◽  
Sarah Bricault ◽  
Marc F. Schmidt
Keyword(s):  
Functional Organization ◽  
Cell Types ◽  
Pattern Generation ◽  
Single Units ◽  
Respiratory Neurons ◽  
Ventrolateral Medulla ◽  
Neural Firing ◽  
Vocal Production ◽  
Ideal System ◽  
Discharge Patterns

Much is known about the neuronal cell types and circuitry of the mammalian respiratory brainstem and its role in normal, quiet breathing. Our understanding of the role of respiration in the context of vocal production, however, is very limited. Songbirds contain a well-defined neural circuit, known as the song system, which is necessary for song production and is strongly coupled to the respiratory system. A major target of this system is nucleus parambigualis (PAm) in the ventrolateral medulla, a structure that controls inspiration by way of its bulbospinal projections but is also an integral part of the song-pattern generation circuit by way of its “thalamocortical” projections to song-control nuclei in the telencephalon. We have mapped out PAm to characterize the cell types and its functional organization. Extracellular single units were obtained in anesthetized adult male zebra finches while measuring air sac pressure to monitor respiration. Single units were characterized by their discharge patterns and the phase of the activity in the respiratory cycle. Several classes of neurons were identified and were analogous to those reported for mammalian medullary respiratory neurons. The majority of the neurons in PAm was classified as inspiratory augmenting or preinspiratory, although other basic discharge patterns were observed as well. The well-characterized connectivity of PAm within the vocal motor circuit and the similarity of its neural firing patterns to the rostral ventral respiratory group and pre-Bötzinger complex of mammals make it an ideal system for investigating the integration of breathing and vocalization.

Ventrolateral medullary respiratory network and a model of cough motor pattern generation

1998 ◽  
Vol 84 (6) ◽  
pp. 2020-2035 ◽  
Author(s):  
Roger Shannon ◽  
David M. Baekey ◽  
Kendall F. Morris ◽  
Bruce G. Lindsey
Keyword(s):  
Motor Pattern ◽  
Pattern Generation ◽  
Nucleus Tractus Solitarii ◽  
Respiratory Neurons ◽  
Generation Model ◽  
Motor Patterns ◽  
Ventral Respiratory Group ◽  
Primary Hypothesis ◽  
Discharge Patterns

The primary hypothesis of this study was that the cough motor pattern is produced, at least in part, by the medullary respiratory neuronal network in response to inputs from “cough” and pulmonary stretch receptor relay neurons in the nucleus tractus solitarii. Computer simulations of a distributed network model with proposed connections from the nucleus tractus solitarii to ventrolateral medullary respiratory neurons produced coughlike inspiratory and expiratory motor patterns. Predicted responses of various “types” of neurons (I-DRIVER, I-AUG, I-DEC, E-AUG, and E-DEC) derived from the simulations were tested in vivo. Parallel and sequential responses of functionally characterized respiratory-modulated neurons were monitored during fictive cough in decerebrate, paralyzed, ventilated cats. Coughlike patterns in phrenic and lumbar nerves were elicited by mechanical stimulation of the intrathoracic trachea. Altered discharge patterns were measured in most types of respiratory neurons during fictive cough. The results supported many of the specific predictions of our cough generation model and suggested several revisions. The two main conclusions were as follows: 1) The Bötzinger/rostral ventral respiratory group neurons implicated in the generation of the eupneic pattern of breathing also participate in the configuration of the cough motor pattern. 2) This altered activity of Bötzinger/rostral ventral respiratory group neurons is transmitted to phrenic, intercostal, and abdominal motoneurons via the same bulbospinal neurons that provide descending drive during eupnea.

Ventilatory responses to cooling the ventrolateral medullary surface of awake and anesthetized goats

1995 ◽  
Vol 78 (1) ◽  
pp. 247-257 ◽  
Author(s):  
P. J. Ohtake ◽  
H. V. Forster ◽  
L. G. Pan ◽  
T. F. Lowry ◽  
M. J. Korducki ◽  
...  
Keyword(s):  
Pulmonary Ventilation ◽  
Respiratory Rhythm ◽  
Respiratory Neurons ◽  
Ventrolateral Medulla ◽  
Arterial Pco2 ◽  
Respiratory Rhythmogenesis ◽  
Ventilatory Responses ◽  
Anesthesia Breathing ◽  
A Site ◽  
Caudal Area

The ventrolateral medulla (VLM) has been reported to be important as a source of tonic facilitation of dorsal respiratory neurons and as a site critical for respiratory rhythmogenesis. We investigated these theories in awake and anesthetized goats (n = 13) by using chronically implanted thermodes to create reversible neuronal dysfunction at superficial VLM sites between the first hypoglossal rootlet and the pontomedullary junction (area M (rostral) and area S). During halothane anesthesia (arterial PCO2 = 57.4 +/- 4.5 Torr), bilateral cooling (thermode temperature = 20 degrees C) of 60–100% of areas M and S for 30 s produced a sustained apnea (46 +/- 4 s) that lasted beyond the period of cooling. While the animals were awake (arterial PCO2 = 36.0 +/- 1.9 Torr), cooling the identical region in the same goats resulted in a decrease (approximately 50%) in pulmonary ventilation, with a brief apnea seen only in one goat. Reductions in both tidal volume and frequency were observed. Qualitatively similar responses were obtained when cooling caudal area M-rostral area S and rostral area M, but the responses were less pronounced. Minimal effects were seen in response to cooling caudal area S. During anesthesia, breathing is critically dependent on superficial VLM neurons, whereas in the awake state these neurons are not essential for the maintenance of respiratory rhythm. Our data are consistent with these superficial VLM neuronal regions providing tonic facilitation to more dorsal respiratory neurons in both the anesthetized and awake states.

Interaction between chemoreceptor and stretch receptor inputs at medullary respiratory neurons

1994 ◽  
Vol 266 (6) ◽  
pp. R1951-R1961 ◽  
Author(s):  
J. Bajic ◽  
E. J. Zuperku ◽  
M. Tonkovic-Capin ◽  
F. A. Hopp
Keyword(s):  
Time Course ◽  
Afferent Input ◽  
Respiratory Neurons ◽  
Neuronal Responses ◽  
Additive Interaction ◽  
Dorsal Respiratory Group ◽  
Afferent Inputs ◽  
Discharge Patterns ◽  
Carotid Body Chemoreceptors ◽  
Common Carotid Arteries

The interaction between afferent inputs from carotid body chemoreceptors (CCRs) and from slowly adapting pulmonary stretch receptors (PSRs) on the discharge patterns of medullary inspiratory (I) and expiratory (E) neurons was characterized in thiopental sodium-anesthetized, paralyzed, ventilated dogs. A cycle-triggered ventilator was used to produce control and test pulmonary afferent input patterns. The CCRs were stimulated by phase-synchronized bolus injections of CO2-saturated saline into the common carotid arteries. Only those neurons whose discharge time course was altered by both inflation and CCR activation were studied. The dorsal respiratory group (DRG) I inflation-insensitive neurons were also included. Cycle-triggered histograms of unit activity were obtained for the neuronal responses to inflation, CO2 bolus, and their combination, as well as for the spontaneous control condition. Linearity of the interaction was tested by comparing the sum of the net individual responses to the net response of the combined afferent inputs. The results suggest that a linear (additive) interaction between CCR and PSR inputs exists for the DRG I inflation-sensitive neurons, the ventral respiratory group (VRG) I decrementing, and caudal VRG E augmenting neurons, while a nonadditive interaction exists for caudal VRG E decrementing bulbospinal neurons. The implications of these findings are discussed.

Hypoxia selectively excites vasomotor neurons of rostral ventrolateral medulla in rats

1994 ◽  
Vol 266 (1) ◽  
pp. R245-R256 ◽  
Author(s):  
M. K. Sun ◽  
D. J. Reis
Keyword(s):  
Sympathetic Nerves ◽  
Rostral Ventrolateral Medulla ◽  
Respiratory Neurons ◽  
Ventrolateral Medulla ◽  
Cellular Mechanisms ◽  
Systemic Hypoxia ◽  
Adequate Stimulus ◽  
Central Oxygen ◽  
Cerebral Ischemic ◽  
Increased Activity

Systemic hypoxia [PaO2 27.3 +/- 1.8 (SE) mmHg] in anesthetized paralyzed rats reversibly increased within seconds the arterial pressure and activities of the sympathetic nerves and the reticulospinal vasomotor neurons of the rostral ventrolateral medulla (RVL). After peripheral chemodenervation, hypoxia also increased activity of the sympathetic nerves and doubled discharges of the vasomotor neurons while inhibiting a majority of the RVL respiratory neurons. Systemic hypercapnia was not effective in eliciting sympathoexcitatory responses. Iontophoresis of sodium cyanide stimulated the vasomotor and inhibited the respiratory neurons. In contrast, iontophoreses of H+, HCO3-, and lactate were without effects on activity of the vasomotor neurons. We conclude 1) hypoxia excites the vasomotor neurons by activating the arterial chemoreceptors and by activating intrinsic cellular mechanisms probably unrelated to accumulation of metabolic byproducts; 2) hypoxia may be the adequate stimulus exciting the RVL-spinal vasomotor and inhibiting the respiratory neurons during the cerebral ischemic response; and 3) these vasomotor neurons may be central oxygen detectors.

Functional Organization of the Endoplasmic Reticulum Dictates the Susceptibility of Target Cells to Arsenite-Induced Mitochondrial Superoxide Formation, Mitochondrial Dysfunction and Apoptosis

2021 ◽  
Author(s):  
Andrea Guidarelli ◽  
Alessia Catalani ◽  
Ersilia Varone ◽  
Stefano Fumagalli ◽  
Ester Zito ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Mitochondrial Dysfunction ◽  
Functional Organization ◽  
Close Contact ◽  
Cell Types ◽  
Target Cells ◽  
Close Apposition ◽  
Mitochondrial Superoxide ◽  
Low Concentrations ◽  
Absolute Requirement

Abstract Arsenite induces many critical effects associated with the formation of reactive oxygen species (ROS) through different mechanisms. We focused on the Ca2+-dependent mitochondrial superoxide (mitoO2-.) formation and addressed questions on the effects of low concentrations of arsenite on the mobilization of the cation from the endoplasmic reticulum and the resulting mitochondrial accumulation. Using various differentiated and undifferentiated cell types uniquely expressing the inositol-1, 4, 5-triphosphate receptor (IP3R), or both the IP3R and the ryanodine receptor (RyR), we determined that expression of this second Ca2+ channel is an absolute requirement for mitoO2-. formation and for the ensuing mitochondrial dysfunction and downstream apoptosis. In arsenite-treated cells, RyR was recruited after IP3R stimulation and agonist studies indicated that in these cells RyR is in close apposition with mitochondria. It was also interesting to observe that arsenite fails to promote mitochondrial Ca2+ accumulation, mitoO2-. formation, mitochondrial toxicity in RyR-devoid cells, in which the IP3R is in close contact with the mitochondria. We therefore conclude that low dose arsenite-induced mitoO2- formation and the resulting mitochondrial dysfunction and toxicity, are prerequisite of cell types expressing the RyR in close apposition with mitochondria.

Control of discharge patterns of medullary respiratory neurons by pulmonary vagal afferent inputs

1987 ◽  
Vol 253 (6) ◽  
pp. R809-R820 ◽  
Author(s):  
E. J. Zuperku ◽  
F. A. Hopp
Keyword(s):  
Linear Functions ◽  
Step Response ◽  
Respiratory Neurons ◽  
Step Frequency ◽  
Test Input ◽  
Linear Relationships ◽  
Vagal Afferent ◽  
The Difference ◽  
Time Courses ◽  
Discharge Patterns

To provide a better understanding of the central mechanisms by which pulmonary afferents reflexly control breathing, the responses of single respiratory neurons to vagal afferent patterns were analyzed. Respiratory-related unit (RRU) recordings were obtained from inspiratory (I), expiratory (E), and phase-spanning neurons in the ventral medulla of halothane-anesthetized, paralyzed, ventilated, vagotomized, mongrel dogs. Electrical stimulation of the largest vagal fibers was used to reflexly alter I and E durations (TI and TE) and to present various temporal input patterns to RRU. The net response was quantified by taking the difference between cycle-triggered histograms (CTH) of activity obtained during an input and the spontaneous control (no input) CTH. For step frequency patterns confined to either the I or E phase, 127 responses in 41 neurons were analyzed. The average step response time was greater than 500 ms. In general the time courses of the control and test-input discharge patterns were linearly related to one another. For I neurons the slopes (beta) of these relationships were linear functions of the vagal step frequency (Fv). Linear relationships were also obtained for 1/TI vs. Fv and 1/beta vs. TI. These results suggest that the vagal control of the discharge patterns of these neurons and phase timing is mediated via a process similar to gain modulation.

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