Topography in the phrenic motoneuron nucleus demonstrated by retrograde multiple-labelling techniques

1990 ◽  
Vol 292 (3) ◽  
pp. 424-434 ◽  
Author(s):  
D. C. Gordon ◽  
F. J. R. Richmond
Keyword(s):  
Phrenic Motoneuron ◽  
Multiple Labelling

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.

Isotope shifts in13C-n.m.r. spectra of18O-labelled acetals; multiple labelling effects at β-carbons

1981 ◽  
pp. 501-502 ◽  
Author(s):  
Richard N. Moore ◽  
James Diakur ◽  
Thomas T. Nakashima ◽  
Sherry L. McLaren ◽  
John C. Vederas
Keyword(s):  
Isotope Shifts ◽  
Multiple Labelling

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.

scholarly journals Phrenic motoneuron discharge patterns following chronic cervical spinal cord injury

2013 ◽  
Vol 249 ◽  
pp. 20-32 ◽  
Author(s):  
Kun-Ze Lee ◽  
Brendan J. Dougherty ◽  
Milapjit S. Sandhu ◽  
Michael A. Lane ◽  
Paul J. Reier ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cervical Spinal Cord ◽  
Cervical Spinal Cord Injury ◽  
Cord Injury ◽  
Phrenic Motoneuron ◽  
Discharge Patterns

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.

scholarly journals Key aspects of phrenic motoneuron and diaphragm muscle development during the perinatal period

2008 ◽  
Vol 104 (6) ◽  
pp. 1818-1827 ◽  
Author(s):  
Carlos B. Mantilla ◽  
Gary C. Sieck
Keyword(s):  
Muscle Development ◽  
Respiratory Muscles ◽  
Motor Units ◽  
Perinatal Period ◽  
Diaphragm Muscle ◽  
Postnatal Maturation ◽  
Motor Behaviors ◽  
Phrenic Motoneurons ◽  
Phrenic Motoneuron ◽  
Key Aspects

At the time of birth, respiratory muscles must be activated to sustain ventilation. The perinatal development of respiratory motor units (comprising an individual motoneuron and the muscle fibers it innervates) shows remarkable features that enable mammals to transition from in utero conditions to the air environment in which the remainder of their life will occur. In addition, significant postnatal maturation is necessary to provide for the range of motor behaviors necessary during breathing, swallowing, and speech. As the main inspiratory muscle, the diaphragm muscle (and the phrenic motoneurons that innervate it) plays a key role in accomplishing these behaviors. Considerable diversity exists across diaphragm motor units, but the determinant factors for this diversity are unknown. In recent years, the mechanisms underlying the development of respiratory motor units have received great attention, and this knowledge may provide the opportunity to design appropriate interventions for the treatment of respiratory disease not only in the perinatal period but likely also in the adult.

scholarly journals Functional Connectivity in the Pontomedullary Respiratory Network

2008 ◽  
Vol 100 (4) ◽  
pp. 1749-1769 ◽  
Author(s):  
Lauren S. Segers ◽  
Sarah C. Nuding ◽  
Thomas E. Dick ◽  
Roger Shannon ◽  
David M. Baekey ◽  
...  
Keyword(s):  
Functional Connectivity ◽  
Respiratory Rhythm ◽  
Ventrolateral Medulla ◽  
Phase Switching ◽  
Functional Connections ◽  
Neuron Populations ◽  
Respiratory Network ◽  
Cross Correlation Analysis ◽  
Respiratory Modulation ◽  
Phrenic Motoneuron

Current models propose that a neuronal network in the ventrolateral medulla generates the basic respiratory rhythm and that this ventrolateral respiratory column (VRC) is profoundly influenced by the neurons of the pontine respiratory group (PRG). However, functional connectivity among PRG and VRC neurons is poorly understood. This study addressed four model-based hypotheses: 1) the respiratory modulation of PRG neuron populations reflects paucisynaptic actions of multiple VRC populations; 2) functional connections among PRG neurons shape and coordinate their respiratory-modulated activities; 3) the PRG acts on multiple VRC populations, contributing to phase-switching; and 4) neurons with no respiratory modulation located in close proximity to the VRC and PRG have widely distributed actions on respiratory-modulated cells. Two arrays of microelectrodes with individual depth adjustment were used to record sets of spike trains from a total of 145 PRG and 282 VRC neurons in 10 decerebrate, vagotomized, neuromuscularly blocked, ventilated cats. Data were evaluated for respiratory modulation with respect to efferent phrenic motoneuron activity and short-timescale correlations indicative of paucisynaptic functional connectivity using cross-correlation analysis and the “gravity” method. Correlogram features were found for 109 (3%) of the 3,218 pairs composed of a PRG and a VRC neuron, 126 (12%) of the 1,043 PRG–PRG pairs, and 319 (7%) of the 4,340 VRC–VRC neuron pairs evaluated. Correlation linkage maps generated for the data support our four motivating hypotheses and suggest network mechanisms for proposed modulatory functions of the PRG.

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