Respiratory neuronal activity during apnea and poststimulatory effects of laryngeal origin in the cat

2000 ◽  
Vol 89 (3) ◽  
pp. 917-925 ◽  
Author(s):  
Fulvia Bongianni ◽  
Donatella Mutolo ◽  
Marco Carfì ◽  
Giovanni A. Fontana ◽  
Tito Pantaleo
Keyword(s):  
Respiratory Depression ◽  
Superior Laryngeal Nerve ◽  
Respiratory Neurons ◽  
Inhibitory Input ◽  
Phase Theory ◽  
Inspiratory Neurons ◽  
Three Phase ◽  
Expiratory Neurons ◽  
Inspiratory Activity ◽  
Respiratory Reflexes

We investigated the behavior of medullary respiratory neurons in cats under pentobarbitone anesthesia, vagotomized, paralysed, and artificially ventilated to elucidate neural mechanisms underlying apnea and poststimulatory respiratory depression induced by superior laryngeal nerve (SLN) stimulation. Inspiratory neurons were completely inhibited during SLN stimulation and poststimulatory apnea. During recovery of inspiratory activity, augmenting inspiratory neurons were depressed, decrementing inspiratory neurons were excited, and late inspiratory neurons displayed unchanged bursts closely locked to the end of the inspiratory phase. Augmenting expiratory neurons were either silenced or displayed different levels of tonic activity during SLN stimulation; some of them were clearly activated. These expiratory neurons displayed activity during poststimulatory apnea, before the onset of the first recovery phrenic burst. Postinspiratory or decrementing expiratory neurons were activated during SLN stimulation; their discharge continued with a decreasing trend during poststimulatory apnea. The results support the three-phase theory of rhythm generation and the view that SLN stimulation provokes a postinspiratory apnea that could represent the inhibitory component of respiratory reflexes of laryngeal origin, such as swallowing. In addition, because a subpopulation of augmenting expiratory neurons displays activation during SLN stimulation, the hypothesis can be advanced that not only postinspiratory, or decrementing expiratory neurons, but also augmenting expiratory neurons may be involved in the genesis of apnea and poststimulatory phenomena. Finally, the increase in the activity of decrementing inspiratory neurons after the end of SLN stimulation may contribute to the generation of poststimulatory respiratory depression by providing an inhibitory input to bulbospinal augmenting inspiratory neurons.

Naloxone attenuates poststimulatory respiratory depression of laryngeal origin in the adult cat

1995 ◽  
Vol 269 (1) ◽  
pp. R113-R123 ◽  
Author(s):  
D. Mutolo ◽  
F. Bongianni ◽  
M. Corda ◽  
G. A. Fontana ◽  
T. Pantaleo
Keyword(s):  
Respiratory Depression ◽  
Time Course ◽  
Superior Laryngeal Nerve ◽  
Endogenous Opioids ◽  
Respiratory Frequency ◽  
Inspiratory Activity ◽  
Stimulation Period ◽  
Adult Cat ◽  
Adult Cats ◽  
Alpha Chloralose

Poststimulatory depression in respiratory activity induced by superior laryngeal nerve (SLN) stimulation was quantitatively investigated in 20 adult cats. The role played in this phenomenon by endogenous opioids was studied using the opiate antagonist naloxone. The effects of hypercapnia on the same phenomenon were also investigated for comparison. Experiments were performed on cats anesthetized with pentobarbitone or alpha-chloralose, vagotomized, paralyzed, and artificially ventilated with 100% O2. Some animals were also carotid sinus denervated. Respiratory output was monitored as integrated phrenic nerve activity. SLN stimulation produced apnea, which outlasted the stimulation period; when respiration resumed, it was markedly depressed as revealed mainly by a decrease in phrenic minute output, respiratory frequency, and rate of rise of inspiratory activity. Phrenic output recovered gradually to control levels following an exponential time course. These effects varied as a function of the duration of SLN stimulation. Naloxone administration (0.8 mg/kg iv) significantly reduced the duration of poststimulatory apnea and attenuated the depression of phrenic minute output of the first recovery breath as a result of changes in peak phrenic activity; it also accelerated the time course of recovery. Hypercapnia did not affect the duration of poststimulatory apnea, but attenuated the initial poststimulatory depression because of changes in respiratory frequency; the rate of recovery was reduced. The results provide characterization of poststimulatory respiratory depression of laryngeal origin in the adult cat and suggest a role of endogenous opioids in its genesis or modulation.

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.

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.

Opioid Action on Respiratory Neuron Activity of the Isolated Respiratory Network in Newborn Rats

2001 ◽  
Vol 95 (3) ◽  
pp. 740-749 ◽  
Author(s):  
Shinhiro Takeda ◽  
Lars I. Eriksson ◽  
Yuji Yamamoto ◽  
Henning Joensen ◽  
Hiroshi Onimaru ◽  
...  
Keyword(s):  
Respiratory Depression ◽  
Opioid Receptor ◽  
Membrane Resistance ◽  
Kappa Opioid Receptor ◽  
Membrane Properties ◽  
Respiratory Neurons ◽  
Kappa Opioid ◽  
Receptor Agonists ◽  
Inspiratory Neurons ◽  
Opioid Receptor Agonists

Background Underlying mechanisms behind opioid-induced respiratory depression are not fully understood. The authors investigated changes in burst rate, intraburst firing frequency, membrane properties, as well as presynaptic and postsynaptic events of respiratory neurons in the isolated brainstem after administration of opioid receptor agonists. Methods Newborn rat brainstem-spinal cord preparations were used and superfused with mu-, kappa-, and delta-opioid receptor agonists. Whole cell recordings were performed from three major classes of respiratory neurons (inspiratory, preinspiratory, and expiratory). Results Mu- and kappa-opioid receptor agonists reduced the spontaneous burst activity of inspiratory neurons and the C4 nerve activity. Forty-two percent of the inspiratory neurons were hyperpolarized and decreased in membrane resistance during opioid-induced respiratory depression. Furthermore, under synaptic block by tetrodotoxin perfusion, similar changes of inspiratory neuronal membrane properties occurred after application of mu- and kappa-opioid receptor agonists. In contrast, resting membrane potential and membrane resistance of preinspiratory and majority of expiratory neurons were unchanged by opioid receptor agonists, even during tetrodotoxin perfusion. Simultaneous recordings of inspiratory and preinspiratory neuronal activities confirmed the selective inhibition of inspiratory neurons caused by mu- and kappa-opioid receptor agonists. Application of opioids reduced the slope of rising of excitatory postsynaptic potentials evoked by contralateral medulla stimulation, resulting in a prolongation of the latency of successive first action potential responses. Conclusions Mu- and kappa-opioid receptor agonists caused reduction of final motor outputs by mainly inhibiting medullary inspiratory neuron network. This inhibition of inspiratory neurons seems to be a result of both a presynaptic and postsynaptic inhibition. The central respiratory rhythm as reflected by the preinspiratory neuron burst rate was essentially unaltered by the agonists.

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.

Pre-Botzinger complex in the cat

1995 ◽  
Vol 73 (4) ◽  
pp. 1452-1461 ◽  
Author(s):  
S. W. Schwarzacher ◽  
J. C. Smith ◽  
D. W. Richter
Keyword(s):  
Spinal Cord ◽  
Neuronal Activity ◽  
Membrane Depolarization ◽  
Neonatal Rat ◽  
Respiratory Neurons ◽  
Spike Discharge ◽  
Inspiratory Phase ◽  
Inspiratory Neurons ◽  
Bötzinger Complex ◽  
Expiratory Neurons

1. Patterns of respiratory neuronal activity were examined in pentobarbitone anesthetized adult cats in a circumscribed area of the ventrolateral medulla, which has previously been defined as the pre-Botzinger complex (pre-BOTC) from electrophysiological and morphological criteria in the brain stem-spinal cord preparation of the neonatal rat. The pre-BOTC has been proposed to play a critical role in respiratory rhythm generation in mammals, but electrophysiological properties of the region have not been thoroughly characterized in the adult brain stem in vivo. 2. From intra- and extracellular recordings, we verified the existence of a well-defined zone with a distinct profile of neuronal activity between the rostral Botzinger complex containing expiratory neurons and the more caudal medullary pool of inspiratory neurons of the ventral respiratory group (VRG) in the para-ambigual region. This zone corresponds to the pre-BOTC. It was characterized by a concentration of the various types of respiratory neurons, particularly those proposed to be involved in respiratory phase transitions, including neurons discharging immediately before the onset of inspiratory phase activity (pre-inspiratory neurons), early-inspiratory, and postinspiratory neurons. The majority of these neurons were presumed interneurons because they were not antidromically activated by spinal cord or cranial nerve stimulation. 3. The locus of the pre-BOTC corresponded histologically to the rostral part of the nucleus ambiguus and ventrolateral reticular formation. It was located caudal to the retrofacial nucleus and rostral to the lateral reticular nucleus, extending 3.0-3.5 mm rostral to the obex, and 3.2-4.0 mm lateral from the midline. This location was homologous to that established in the neonatal rat. 4. Pre-inspiratory neurons (pre-I neurons) were specifically found in the pre-BOTC. Intracellular recordings from these neurons revealed two types of activity patterns. Type 1 of pre-I neurons exhibited a steady membrane depolarization during expiration and a steep membrane depolarization with a high-frequency burst of action-potential discharge during the phase transition from expiration to inspiration. This was followed by a decline of depolarization and spike discharge during the remainder of the inspiratory phase. A second type of pre-I neurons exhibited a secondary graded membrane depolarization and burst discharge during the late-inspiratory period. 5. Synaptic events were examined in other respiratory neurons during the 40-160 ms preceding the onset of phrenic nerve activity when pre-I neurons exhibited peak spike discharge. Early-inspiratory, throughout-respiratory, and postinspiratory neurons were disinhibited during this period, whereas stage-2 expiratory neurons exhibited a decrease in spike activity and repolarization.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Neural Mechanisms of Sevoflurane-induced Respiratory Depression in Newborn Rats

2008 ◽  
Vol 109 (2) ◽  
pp. 233-242 ◽  
Author(s):  
Junya Kuribayashi ◽  
Shigeki Sakuraba ◽  
Masanori Kashiwagi ◽  
Eiki Hatori ◽  
Miki Tsujita ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Respiratory Depression ◽  
Motor Neurons ◽  
Type A ◽  
Aminobutyric Acid ◽  
Respiratory Neurons ◽  
Gamma Aminobutyric Acid ◽  
Inspiratory Neurons ◽  
Acid Type ◽  
Bötzinger Complex

Background Sevoflurane-induced respiratory depression has been reported to be due to the action on medullary respiratory and phrenic motor neurons. These results were obtained from extracellular recordings of the neurons. Here, the authors made intracellular recordings of respiratory neurons and analyzed their membrane properties during sevoflurane application. Furthermore, they clarified the role of gamma-aminobutyric acid type A receptors in sevoflurane-induced respiratory depression. Methods In the isolated brainstem-spinal cord of newborn rat, the authors recorded the C4 nerve burst as an index of inspiratory activity. The preparation was superfused with a solution containing sevoflurane alone or sevoflurane plus the gamma-aminobutyric acid type A receptor antagonist picrotoxin or bicuculline. Neuronal activities were also recorded using patch clamp techniques. Results Sevoflurane decreased C4 burst rate and amplitude. Separate perfusion of sevoflurane to the medulla and to the spinal cord decreased C4 burst rate and amplitude, respectively. Both picrotoxin and bicuculline attenuated the reduction of C4 burst rate. Sevoflurane reduced both intraburst firing frequency and membrane resistance of respiratory neurons except for inspiratory neurons. Conclusion Under the influence of sevoflurane, the region containing inspiratory neurons, i.e., the pre-Bötzinger complex, may determine the inspiratory rhythm, because reduced C4 bursts were still synchronized with the bursts of inspiratory neurons within the pre-Bötzinger complex. In contrast, the sevoflurane-induced decrease in C4 burst amplitude is mediated through the inhibition of phrenic motor neurons. gamma-Aminobutyric acid type A receptors may be involved in the sevoflurane-induced respiratory depression within the medulla, but not within the spinal cord.

Activity of respiratory neurons during hypoxia in the chemodenervated cat

1995 ◽  
Vol 78 (3) ◽  
pp. 856-861 ◽  
Author(s):  
S. J. England ◽  
J. E. Melton ◽  
M. A. Douse ◽  
J. Duffin
Keyword(s):  
Respiratory Depression ◽  
Late Onset ◽  
Respiratory Neurons ◽  
Ventral Respiratory Group ◽  
Inspiratory Neurons ◽  
Dorsal Respiratory Group ◽  
Premotor Neurons ◽  
Acute Hypoxic Hypoxia ◽  
Subsequent Loss ◽  
Initial Depression

Exposure of anesthetized paralyzed vagotomized peripherally chemodenervated cats to hypoxia results in initial depression and subsequent loss of the phrenic neurogram. To determine whether hypoxic respiratory depression results from the inhibition of respiratory premotor neurons by bulbospinal neurons of the Botzinger complex (Bot-E neurons), extracellular recordings were made of dorsal and ventral respiratory group bulbospinal inspiratory neurons and Bot-E neurons during acute hypoxic hypoxia. All neurons recorded decreased firing rate during hypoxia. Bot-E neurons became silent before the loss of phasic phrenic activity during hypoxia and commenced firing before or coincident with the return of the phrenic neurogram during reoxygenation. Inspiratory neurons ceased firing coincident with phrenic silence. Dorsal respiratory group and ventral respiratory group neurons that had a late onset of firing with respect to the phrenic neurogram during normoxia fired progressively earlier in inspiration during hypoxia, an effect that was reversed during reoxygenation. These data are consistent with inhibition and/or disfacilitation as the mechanism of hypoxic respiratory depression but suggest that Bot-E neurons are not the source of this inhibition.

Sign in / Sign up

Export Citation Format

Share Document