Respiratory neurons in the medulla of the rabbit: distribution, discharge patterns and spinal projections

1991 ◽  
Vol 541 (2) ◽  
pp. 284-292 ◽  
Author(s):  
Chun Jiang ◽  
Eh Shen
Keyword(s):  
Respiratory Neurons ◽  
Discharge Patterns

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.

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.

Chest wall distortion and discharge of pulmonary slowly adapting receptors

1992 ◽  
Vol 73 (4) ◽  
pp. 1619-1625 ◽  
Author(s):  
S. Iscoe ◽  
S. P. Gordon
Keyword(s):  
Smooth Muscle ◽  
Chest Wall ◽  
Airway Smooth Muscle ◽  
Muscle Tone ◽  
Respiratory Neurons ◽  
Lung Inflation ◽  
Smooth Muscle Tone ◽  
Residual Capacity ◽  
Discharge Patterns ◽  
Spontaneously Breathing

We assessed the effects of chest wall distortion, changes in lung volume, and abolition of airway smooth muscle tone on the discharge patterns of 92 pulmonary slowly adapting receptors (SAR) in decerebrate, spontaneously breathing cats. Distortion resulted from their inspiratory efforts against an occluded airway at functional residual capacity and at increased end-expiratory lung volumes. Approximately 40% of SAR increased discharge frequencies during occlusions. Modulation of SAR discharge during occlusions persisted after administration of atropine to eliminate airway smooth muscle tone. Phasic modulation of SAR discharge was eliminated during no-inflation tests after paralyzing the cats and ventilating them on a cycle-triggered pump. We conclude 1) parasympathetic modulation of airway smooth muscle tone makes no obvious contribution to SAR discharge in spontaneously breathing cats; 2) the no-inflation test (withholding of lung inflation during neural inspiration) in paralyzed and ventilated cats is a valid test for the presence of projections from SAR to medullary respiratory neurons; and 3) in the absence of tidal volume changes, distortion stimulates some SAR. Sensory feedback from receptors in the lung, not just those in the chest wall, may therefore provide information about abnormal chest wall configurations.

Differential Effects of GABAA Receptor Antagonists in the Control of Respiratory Neuronal Discharge Patterns

1998 ◽  
Vol 80 (5) ◽  
pp. 2368-2377 ◽  
Author(s):  
Z. Dogas ◽  
M. Krolo ◽  
E. A. Stuth ◽  
M. Tonkovic-Capin ◽  
F. A. Hopp ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Discharge Rate ◽  
Active Phase ◽  
Respiratory Neurons ◽  
Receptor Antagonists ◽  
Inhibitory Neurotransmitter ◽  
Differential Effects ◽  
Tonic Level ◽  
Silent Phase ◽  
Discharge Patterns

Dogas, Z., M. Krolo, E. A. Stuth, M. Tonkovic-Capin, F. A. Hopp, D. R. McCrimmon, and E. J. Zuperku. Differential effects of GABAA receptor antagonists in the control of respiratory neuronal discharge patterns. J. Neurophysiol. 80: 2368–2377, 1998. To ascertain the role of the inhibitory neurotransmitter γ-aminobutyric acid (GABA) in shaping and controlling the phasic discharge patterns of medullary respiratory premotor neurons, localized pressure applications of the competitive GABAA receptor antagonist bicuculline (BIC) and the noncompetitive GABAA receptor antagonist picrotoxin (PIC) were studied. Multibarrel micropipettes were used in halothane anesthetized, paralyzed, ventilated, vagotomized dogs to record single unit activity from inspiratory and expiratory neurons in the caudal ventral respiratory group and to picoeject GABAA receptor antagonists. The moving time average of phrenic nerve activity was used to determine respiratory phase durations and to synchronize cycle-triggered histograms of discharge patterns. Picoejection of BIC and PIC had qualitatively different effects on the discharge patterns of respiratory neurons. BIC caused an increase in the discharge rate during the neuron's active phase without inducing activity during the neuron's normally silent phase. The resulting discharge patterns were amplified replicas (×2–3) of the underlying preejection phasic patterns. In contrast, picoejection of PIC did not increase the peak discharge rate during the neuron's active phase but induced a tonic level of activity during the neuron's normally silent phase. The maximum effective BIC dose (15 ± 1.8 pmol/min) was considerably smaller than that for PIC (280 ± 53 pmol/min). These findings suggest that GABAA receptors with differential pharmacology mediate distinct functions within the same neuron, 1) gain modulation that is BIC sensitive but PIC insensitive and 2) silent-phase inhibition blocked by PIC. These studies also suggest that the choice of an antagonist is an important consideration in the determination of GABA receptor function within the respiratory motor control system.

Differential Modulation of Respiratory Neuronal Discharge Patterns by GABAA Receptor and Apamin-Sensitive K+ Channel Antagonism

2001 ◽  
Vol 86 (5) ◽  
pp. 2363-2373 ◽  
Author(s):  
V. Tonkovic-Capin ◽  
A. G. Stucke ◽  
E. A. Stuth ◽  
M. Tonkovic-Capin ◽  
M. Krolo ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Respiratory Neurons ◽  
K Channel ◽  
Induced Response ◽  
Gaba Uptake ◽  
Gain Modulation ◽  
Sk Channels ◽  
Drug Induced ◽  
Nipecotic Acid ◽  
Discharge Patterns

The discharge patterns of respiratory neurons of the caudal ventral respiratory group (cVRG) appear to be subject to potent GABAergic gain modulation. Local application of the GABAA receptor antagonist bicuculline methochloride amplifies the underlying discharge frequency ( F n) patterns mediated by endogenous excitatory and inhibitory synaptic inputs. Gain modulation can also be produced by alterations in the amplitude of spike afterhyperpolarizations (AHPs) mediated by apamin-sensitive small-conductance Ca2+-activated K+ (SK) channels. Since methyl derivatives of bicuculline (BICm) also have been shown to reduce the amplitude of AHPs, in vitro, it is possible that the BICm-induced gain modulation is due to a block of SK channels. The purpose of these studies was to determine the mechanisms by which BICm produces gain modulation and to characterize the influence of SK channels in the control of respiratory neuron discharge. Six protocols were used in this in vivo study of cVRG inspiratory (I) and expiratory (E) neurons in decerebrate, paralyzed, ventilated dogs. The protocols included characterizations of the neuronal responses to 1) BICm and apamin on the same neuron, 2) BICm during maximum apamin-induced block of AHPs, 3) apamin during maximum BICm-induced gain modulatory responses, 4) the specific GABAAreceptor antagonist, (+)β-hydrastine, 5) the specific GABAA receptor agonist, muscimol, and 6) the GABA uptake inhibitor, nipecotic acid. For protocols 3, 5, and 6, only E neurons were studied. Four-barrel micropipettes were used for extracellular single neuron recording and pressure ejection of drugs. Cycle-triggered histograms were used to quantify the F n patterns and to determine the drug-induced changes in the gain (slope) and offset of the F n patterns. Compared to apamin at maximum effective dose rates, BICm produced a 2.1-fold greater increase in peak F n and a 3.1-fold greater increase in average F n. BICm and apamin produced similar increases in gain, but the offsets due to apamin were more negative. The responses to hydrastine were similar to BICm. During maximum apamin block, BICm produced an additional 112 ± 22% increase in peak F n. Conversely, apamin produced an additional 176 ± 74% increase in peak F n during the maximum BICm-induced response. Muscimol and nipecotic acid both decreased the gain and offset of the discharge patterns. Taken together, these results suggest that the gain modulatory effect of BICm is due to a reduction of GABAA-ergic shunting inhibition rather than a reduction in AHPs by block of SK channels in canine cVRG neurons.

Cerebellar control of expiratory activities of medullary neurons and spinal nerves

1993 ◽  
Vol 74 (4) ◽  
pp. 1934-1940 ◽  
Author(s):  
Q. Huang ◽  
D. Zhou ◽  
W. M. St John
Keyword(s):  
Respiratory Neurons ◽  
Spinal Motoneurons ◽  
Spinal Neurons ◽  
Spinal Nerves ◽  
Interposed Nucleus ◽  
Neural Activities ◽  
Medullary Respiratory Neurons ◽  
Discharge Patterns ◽  
Medullary Neurons ◽  
Stimulation Of

Expiratory-related activities of spinal nerves are augmented after stimulation of the infracerebellar nucleus of the cerebellum. These stimulations alter neither inspiratory spinal neural activities nor inspiratory and expiratory laryngeal neural activities. It was hypothesized that efferents from the infracerebellar nucleus impinge on spinal motoneurons by a pathway that bypasses the medulla. In decerebrate, paralyzed, and vagotomized cats, phrenic and expiratory triangularis sterni activities and activities of medullary respiratory neurons were recorded. During infracerebellar stimulation, activities increased for expiratory bulbospinal neurons and neurons with tonic discharge patterns. After unilateral ablation of the infracerebellar nucleus by kainic acid, triangularis sterni discharge was eliminated and activities of expiratory bulbospinal neurons continued at reduced frequencies. Stimulations of the anterior interposed nucleus caused both inspiratory and expiratory activities to increase, whereas no systematic changes followed stimulations of the vermis. Results establish that at least a portion of the changes in expiratory activities of spinal motoneurons after perturbations of the infracerebellar nucleus occurs secondarily to changes in activities of medullary neurons. The possibility of separate cerebellar projections to medullary and spinal neurons is discussed.

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