Excitatory connections between upper cervical inspiratory neurons and phrenic motoneurons in cats

1994 ◽  
Vol 77 (2) ◽  
pp. 679-683 ◽  
Author(s):  
Y. Nakazono ◽  
M. Aoki
Keyword(s):  
Phrenic Nerve ◽  
Respiratory Neurons ◽  
Transmission Delays ◽  
Phrenic Motoneurons ◽  
Inspiratory Neurons ◽  
Upper Cervical ◽  
Cervical Segment ◽  
Focal Cooling ◽  
Descending Influences ◽  
Phrenic Motoneuron

This study aimed to determine whether upper cervical inspiratory neurons (UCINs), which are localized in the intermediolateral part of the gray matter of the upper cervical segments, have propriospinal connections to phrenic motoneurons of the ipsilateral lower cervical segment in anesthetized cats. Unit action potentials of UCINs were extracellularly recorded simultaneously with ipsilateral phrenic nerve activity. To eliminate the descending influences from medullary respiratory neurons to phrenic motoneurons, bulbospinal conduction paths were temporarily blocked by focal cooling applied to the ventral caudal medulla at the pyramidal decussation level by means of a cooling thermode (1 mm tip diam). By using a spike-triggered method, during cooling phrenic nerve activities were evoked by UCIN spikes that were elicited by microinjection of L-glutamate for 20 of the 55 (36%) UCIN units examined. The onset latencies of these phrenic motoneuron responses ranged from 1.5 to 7.1 ms (mean 3.6 ms), depending on synaptic transmission delays. These results clearly demonstrate that UCINs have, at least in part, excitatory mono- and paucisynaptic connections with ipsilateral phrenic motoneurons.

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.

scholarly journals Phrenic Motoneuron Discharge Patterns During Hypoxia-Induced Short-Term Potentiation in Rats

2009 ◽  
Vol 102 (4) ◽  
pp. 2184-2193 ◽  
Author(s):  
Kun-Ze Lee ◽  
Paul J. Reier ◽  
David D. Fuller
Keyword(s):  
Phrenic Nerve ◽  
Cell Types ◽  
Progressive Increase ◽  
Short Term ◽  
Phrenic Motoneurons ◽  
Term Potentiation ◽  
Discharge Duration ◽  
Phrenic Motoneuron ◽  
Discharge Patterns ◽  
Increased Activity

Hypoxia-induced short-term potentiation (STP) of respiratory motor output is manifested by a progressive increase in activity after the acute hypoxic response and a gradual decrease in activity on termination of hypoxia. We hypothesized that STP would be differentially expressed between physiologically defined phrenic motoneurons (PhrMNs). Phrenic nerve “single fiber” recordings were used to characterize PhrMN discharge in anesthetized, vagotomized and ventilated rats. PhrMNs were classified as early (Early-I) or late inspiratory (Late-I) according to burst onset relative to the contralateral phrenic neurogram during normocapnic baseline conditions. During hypoxia (FIO2 = 0.12–0.14, 3 min), both Early-I and Late-I PhrMNs abruptly increased discharge frequency. Both cell types also showed a progressive increase in frequency over the remainder of hypoxia. However, Early-I PhrMNs showed reduced overall discharge duration and total spikes/breath during hypoxia, whereas Late-I PhrMNs maintained constant discharge duration and therefore increased the number of spikes/breath. A population of previously inactive (i.e., silent) PhrMNs was recruited 48 ± 8 s after hypoxia onset. These PhrMNs had a Late-I onset, and the majority (8/9) ceased bursting promptly on termination of hypoxia. In contrast, both Early-I and Late-I PhrMNs showed post-hypoxia STP as reflected by greater discharge frequencies and spikes/breath during the post-hypoxic period ( P < 0.01 vs. baseline). We conclude that the expression of phrenic STP during hypoxia reflects increased activity in previously active Early-I and Late-I PhrMNs and recruitment of silent PhrMNs. post-hypoxia STP primarily reflects persistent increases in the discharge of PhrMNs, which were active before hypoxia.

Comparison of phrenic motoneuron responses to hypercapnia and isocapnic hypoxia

1979 ◽  
Vol 46 (6) ◽  
pp. 1096-1102 ◽  
Author(s):  
W. M. St John ◽  
D. Bartlett
Keyword(s):  
Unit Activity ◽  
Phrenic Nerve ◽  
Interspike Interval ◽  
Activity Patterns ◽  
Nerve Fibers ◽  
Respiratory Cycle ◽  
Efferent Activity ◽  
Phrenic Motoneurons ◽  
Phrenic Motoneuron ◽  
Decerebrate Cats

This study was undertaken to compare phrenic motoneuron responses to hypercapnia and isocapnic hypoxia. Efferent activity of single phrenic nerve fibers was recorded with that of the contralateral phrenic nerve in decerebrate cats which were vagotomized, paralyzed, and artificially ventilated. At normocapnia in hyperoxia, single phrenic fibers were distributed into approximately equal “early” and “late” populations according to their onset of activity relative to the period of the phrenic burst. Elevations of PACO2 or diminutions of PAO2 resulted in progressive increases in the number of spikes per respiratory cycle and decreases in the modal interspike interval for both early and late units. Moreover, either stimulus caused an onset of late unit activity at progressively earlier portions of inspiration. At equivalent levels of peak integrated phrenic discharge achieved at normocapnia or hypercapnia as compared to normoxia or hypoxia, there were no differences in activity patterns for either early or late units. It is concluded that hypoxia-induced alterations in the activity of single phrenic motoneurons are identical to those changes resulting from hypercapnia.

Phrenic motoneuron discharge during sustained inspiratory resistive loading

1996 ◽  
Vol 81 (5) ◽  
pp. 2260-2266 ◽  
Author(s):  
Steve Iscoe
Keyword(s):  
Phrenic Nerve ◽  
Transdiaphragmatic Pressure ◽  
Phrenic Motoneurons ◽  
Resistive Loading ◽  
Instantaneous Discharge ◽  
Unidentified Source ◽  
Phrenic Motoneuron ◽  
Discharge Patterns ◽  
End Tidal ◽  
Spontaneously Breathing

Iscoe, Steve. Phrenic motoneuron discharge during sustained inspiratory resistive loading. J. Appl. Physiol. 81(5): 2260–2266, 1996.—I determined whether prolonged inspiratory resistive loading (IRL) affects phrenic motoneuron discharge, independent of changes in chemical drive. In seven decerebrate spontaneously breathing cats, the discharge patterns of eight phrenic motoneurons from filaments of one phrenic nerve were monitored, along with the global activity of the contralateral phrenic nerve, transdiaphragmatic pressure, and fractional end-tidal CO2 levels. Discharge patterns during hyperoxic CO2 rebreathing and breathing against an IRL (2,500–4,000 cmH2O ⋅ l−1 ⋅ s) were compared. During IRL, transdiaphragmatic pressure increased and then either plateaued or decreased. At the highest fractional end-tidal CO2 common to both runs, instantaneous discharge frequencies in six motoneurons were greater during sustained IRL than during rebreathing, when compared at the same time after the onset of inspiration. These increased discharge frequencies suggest the presence of a load-induced nonchemical drive to phrenic motoneurons from unidentified source(s).

Comparison of phrenic motoneuron activity during eupnea and gasping

1981 ◽  
Vol 50 (5) ◽  
pp. 994-998 ◽  
Author(s):  
W. M. St John ◽  
D. Bartlett
Keyword(s):  
Phrenic Nerve ◽  
Action Potentials ◽  
Single Fiber ◽  
Discharge Frequency ◽  
Fiber Types ◽  
Unit Discharge ◽  
Phrenic Motoneurons ◽  
Motoneuron Activity ◽  
Phrenic Motoneuron ◽  
Pontomedullary Junction

Single-fiber phrenic nerve action potentials were recorded together with activity of contralateral whole phrenic nerve rootlets during eupnea and gasping in decerebrate, cerebellectomized, vagotomized, paralyzed, and ventilated cats. Gasping was reversibly produced by cooling a fork thermode positioned through the pontomedullary junction. In eupnea, phrenic motoneurons were distributed into "early" and "late" populations relative to their onset of activity during inspiration. During gasping, however, both fiber types typically commenced activity at the beginning of the phrenic nerve burst. Moreover, late fibers, but not early units, exhibited an augmentation of discharge frequency with the onset of gasping. The concentration of activity of all phrenic motoneurons at the beginning of inspiration and the increase in late-unit discharge frequency account for the faster rise of the gasp as compared with the eupneic breath. It is concluded that the pattern of phrenic nerve activation during gasping differs fundamentally from that during eupnea. These results support the concept that mechanisms underlying the neurogenesis of gasping and eupnea may not be identical.

Effects of abdominal or cardiopulmonary sympathetic afferents on upper cervical inspiratory neurons

2000 ◽  
Vol 278 (5) ◽  
pp. R1289-R1295 ◽  
Author(s):  
Y. Yuan ◽  
M. J. Chandler ◽  
R. D. Foreman ◽  
J. P. Farber
Keyword(s):  
Phrenic Nerve ◽  
Splanchnic Nerve ◽  
Biphasic Response ◽  
Nerve Activity ◽  
Response Latencies ◽  
Extracellular Recordings ◽  
Phrenic Nerve Activity ◽  
Inspiratory Neurons ◽  
Upper Cervical ◽  
Greater Splanchnic Nerve

Responses of upper cervical inspiratory neurons (UCINs) to abdominal visceral or cardiopulmonary sympathetic stimulation were studied using extracellular recordings from 213 UCINs in 54 pentobarbital sodium-anesthetized and paralyzed rats. Phrenic nerve activity was used to assess inspiration. The UCINs discharging during inspiration only were mainly in the C1 segment, whereas phase-spanning UCINs were mostly in the C2 segment. Phase-spanning activity was typically retained after overventilation or vagotomy. When greater splanchnic nerve (GSN) or cardiopulmonary sympathetic afferent (CPSA) fibers were electrically stimulated, augmented UCIN activity was observed in 65% of cells responding to CPSA stimulation but in only 17% of cells responding to GSN. Response latencies were 10.7 ± 0.5 and 20.6 ± 1.5 (SE) ms, respectively. Many augmented responses to CPSA stimulation (64%) and all augmented responses to GSN stimulation were followed by suppression of UCIN discharge (biphasic response). Phrenic nerve activity was suppressed by both GSN and CPSA stimulation, but with shorter latency for the latter (29 ± 0.7 vs. 14.0 ± 0.7 ms). Excitation of UCINs using CPSA stimulation occurs more often and by a more direct pathway than for GSN input.

Delayed poststimulus decrease of phrenic motoneuron output produced by phrenic nerve afferent stimulation

1993 ◽  
Vol 74 (1) ◽  
pp. 68-72 ◽  
Author(s):  
J. D. Road ◽  
S. Osborne ◽  
Y. Wakai
Keyword(s):  
Phrenic Nerve ◽  
Similar Response ◽  
Thin Fiber ◽  
Afferent Nerves ◽  
Bilateral Carotid ◽  
Muscle Afferent ◽  
Anesthetized Dogs ◽  
Phrenic Motoneuron ◽  
End Tidal ◽  
Stimulation Of

The immediate effects of phrenic afferent nerve activation on ventilation have been shown to be both excitatory and inhibitory. Long-lasting inhibitory effects on respiratory motoneuron output have been reported after stimulation of afferent nerves from limb muscles. However, whether respiratory muscle afferent nerves can produce this effect is unknown. We therefore hypothesized that activation of phrenic afferent nerves may produce a prolonged decrease of respiratory motoneuron output. Six alpha-chloralose-anesthetized dogs were studied after vagotomy and bilateral carotid sinus nerve section. The dogs were paralyzed, and end-tidal CO2 was controlled by mechanical ventilation. The proximal end of the cut thoracic phrenic nerve was electrically stimulated for 1 min at intensities that produced activation of thin-fiber afferents. The contralateral efferent phrenic integrated electroneurogram (ENG) was recorded. During stimulation, phrenic ENG activity increased. ENG activity was recorded during recovery and reached a peak decrease compared with control of 19 +/- 11% (SD) 9.0 +/- 6 min after stimulation and returned to control after 30 min. A qualitatively similar response was seen after stimulation of the gastrocnemius nerve. We conclude that activation of thin-fiber afferents in the phrenic nerve can produce a delayed and prolonged decrease of respiratory motoneuron output similar to that of limb muscle afferent nerves.

Responses of bulbospinal and laryngeal respiratory neurons to hypercapnia and hypoxia

1985 ◽  
Vol 59 (4) ◽  
pp. 1201-1207 ◽  
Author(s):  
W. M. St John ◽  
A. L. Bianchi
Keyword(s):  
Spinal Cord ◽  
Recurrent Laryngeal Nerve ◽  
Phrenic Nerve ◽  
Action Potentials ◽  
Respiratory Muscles ◽  
Laryngeal Nerve ◽  
Respiratory Neurons ◽  
Peripheral Chemoreceptor ◽  
Medullary Respiratory Neurons ◽  
Neuronal Groups

The purpose was to evaluate activities of medullary respiratory neurons during equivalent changes in phrenic discharge resulting from hypercapnia and hypoxia. Decerebrate, cerebellectomized, paralyzed, and ventilated cats were used. Vagi were sectioned at left midcervical and right intrathoracic levels caudal to the origin of right recurrent laryngeal nerve. Activities of phrenic nerve and single respiratory neurons were monitored. Neurons exhibiting antidromic action potentials following stimulations of the spinal cord and recurrent laryngeal nerve were designated, respectively, bulbospinal or laryngeal. The remaining neurons were not antidromically activated. Hypercapnia caused significant augmentations of discharge frequencies for all neuronal groups. Many of these neurons had no change or declines of activity in hypoxia. We conclude that central chemoreceptor afferent influences are ubiquitous, but excitatory influences from carotid chemoreceptors are more limited in distribution among medullary respiratory neurons. Hypoxia will increase activities of neurons that receive sufficient excitatory peripheral chemoreceptor afferents to overcome direct depression by brain stem hypoxia. The possibility that responses of respiratory muscles to hypoxia are programmed within the medulla is discussed.

Phrenic and external intercostal motoneuron activity during progressive asphyxia

1987 ◽  
Vol 63 (4) ◽  
pp. 1413-1420 ◽  
Author(s):  
G. Macefield ◽  
B. Nail
Keyword(s):  
Duty Cycle ◽  
Instantaneous Frequency ◽  
Phrenic Nerve ◽  
Artificial Ventilation ◽  
Phrenic Motoneurons ◽  
Inspiratory Activity ◽  
Motoneuron Activity ◽  
Intercostal Nerves

Phrenic and external intercostal motoneuron activities were compared during progressive asphyxia induced by the interruption of artificial ventilation in the pentobarbital-urethan-anesthetized, gallamine-paralysed rabbit. The relative augmentation of inspiratory activity of the T1-T4 external intercostal nerves was significantly greater than that of the phrenic nerve during asphyxic hyperpnea. This was associated with a greater recruitment of intercostal than of phrenic motoneurons, particularly late in the hyperpneic phase immediately before the period of asphyxic apnea. However, peak and average discharge frequencies developed by intercostal motoneurons (n = 20) were only approximately 60% of those of the phrenic motoneurons (n = 28). Gasping respiration terminated the apneic period and was associated with a further intense recruitment of intercostal though not of phrenic motoneurons, but discharge frequencies developed by the intercostal motoneurons remained approximately 60% of those of the phrenic motoneurons. The instantaneous frequency profiles generated by the motoneurons often exhibited progressive changes during the terminal stages of hyperpnea (reduction in inspiratory duration and duty cycle and increases in inspiratory slope and discharge frequencies) such that much of the character of gasping respiration became evident before the apnea. Such smooth transitional sequences do not obviate the existence of an “independent gasping center” but do require that such a proposed center at least possess the capacity for interaction with those sites responsible for the generation of eupneic and hyperpneic respiration.

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