Synaptic Inhibition of Cat Phrenic Motoneurons by Internal Intercostal Nerve Stimulation

1999 ◽  
Vol 82 (3) ◽  
pp. 1224-1232 ◽  
Author(s):  
Mark C. Bellingham
Keyword(s):  
Phrenic Nerve ◽  
Intercostal Nerve ◽  
Evoked Responses ◽  
Nerve Activity ◽  
Synaptic Inputs ◽  
Phrenic Nerve Activity ◽  
Reflex Pathways ◽  
Phrenic Motoneurons ◽  
Conditioning Stimuli ◽  
Stimulation Of

Intracellular recordings from 65 phrenic motoneurons (PMNs) in the C5 segment and recordings of C5 phrenic nerve activity were made in 27 pentobarbitone-anesthetized, paralyzed, and artificially ventilated adult cats. Inhibition of phrenic nerve activity and PMN membrane potential hyperpolarization (48/55 PMNs tested) was seen after stimulation of the internal intercostal nerve (IIN) at a mean latency to onset of 10.3 ± 2.7 ms. Reversal of IIN-evoked hyperpolarization ( n = 14) by injection of negative current or diffusion of chloride ions occurred in six cases, and the hyperpolarization was reduced in seven others. Stimulation of the IIN thus activates chloride-dependent inhibitory synaptic inputs to most PMNs. The inhibitory phrenic nerve response to IIN stimulation was reduced by ipsilateral transection of the lateral white matter at the C3 level and was converted to an excitatory response by complete ipsilateral cord hemisection at the same level. After complete ipsilateral hemisection of the spinal cord at C3 level, stimulation of the IIN evoked both excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) in PMNs ( n = 10). It was concluded that IIN stimulation can evoke both excitatory and inhibitory responses in PMNs using purely spinal circuitry, but that excitatory responses are normally suppressed by a descending pathway in intact animals. Fifteen PMNs were tested for possible presynaptic convergence of inputs in these reflex pathways, using test and conditioning stimuli. Significant enhancement (>20%) of IPSPs were seen in seven of eight IIN-evoked responses using pericruciate sensorimotor cortex (SMC) conditioning stimuli, but only one of five IIN-evoked responses were enhanced by superior laryngeal nerve (SLN) conditioning stimuli. The IIN-evoked IPSP was enhanced in one of two motoneurons by stimulation of the contralateral phrenic nerve. It was concluded that presynaptic interneurons were shared by the IIN and SMC pathways, but uncommonly by other pathways. These results indicate that PMNs receive inhibitory synaptic inputs from ascending thoracocervical pathways and from spinal interneurons. These inhibitory reflex pathways activated by afferent inputs from the chest wall may play a significant role in the control of PMN discharge, in parallel with disfacilitation following reduced activity in bulbospinal neurons projecting to PMNs.

Daily acute intermittent hypoxia enhances phrenic motor output and stimulus-evoked phrenic responses in rats

2021 ◽  
Author(s):  
Raphael Rodrigues Perim ◽  
Michael D. Sunshine ◽  
Joseph F. Welch ◽  
Juliet Santiago ◽  
Ashley Holland ◽  
...  
Keyword(s):  
Motor Neurons ◽  
Phrenic Nerve ◽  
Intermittent Hypoxia ◽  
Neural Control ◽  
Respiratory Cycle ◽  
Evoked Responses ◽  
Nerve Activity ◽  
Synaptic Inputs ◽  
Phrenic Nerve Activity ◽  
The Impact

Plasticity is a hallmark of the respiratory neural control system. Phrenic long-term facilitation (pLTF) is one form of respiratory plasticity characterized by persistent increases in phrenic nerve activity following acute intermittent hypoxia (AIH). Although there is evidence that key steps in the cellular pathway giving rise to pLTF are localized within phrenic motor neurons (PMNs), the impact of AIH on the strength of breathing-related synaptic inputs to PMNs remains unclear. Further, the functional impact of AIH is enhanced by repeated/daily exposure to AIH (dAIH). Here, we explored the effects of AIH vs. 2 weeks of dAIH preconditioning on spontaneous and evoked responses recorded in anesthetized, paralyzed (with pancuronium bromide) and mechanically ventilated rats. Evoked phrenic potentials were elicited by respiratory cycle-triggered lateral funiculus stimulation at C2 delivered prior to- and 60 min post-AIH (or an equivalent time in controls). Charge-balanced biphasic pulses (100 µs/phase) of progressively increasing intensity (100 to 700 µA) were delivered during the inspiratory and expiratory phases of the respiratory cycle. Although robust pLTF (~60% from baseline) was observed after a single exposure to moderate AIH (3 x 5 min; 5 min intervals), there was no effect on evoked phrenic responses, contrary to our initial hypothesis. However, in rats preconditioned with dAIH, baseline phrenic nerve activity and evoked responses were increased, suggesting that repeated exposure to AIH enhances functional synaptic strength when assessed using this technique. The impact of daily AIH preconditioning on synaptic inputs to PMNs raises interesting questions that require further exploration.

Effect of electric and chemical stimulation of the raphe obscurus on phrenic nerve activity in the cat

1986 ◽  
Vol 362 (2) ◽  
pp. 214-220 ◽  
Author(s):  
Joseph R. Holtman ◽  
Nancy C. Anastasi ◽  
Wesley P. Norman ◽  
Kenneth L. Dretchen
Keyword(s):  
Phrenic Nerve ◽  
Chemical Stimulation ◽  
Nerve Activity ◽  
Phrenic Nerve Activity ◽  
Stimulation Of

scholarly journals Midcervical neuronal discharge patterns during and following hypoxia

2015 ◽  
Vol 113 (7) ◽  
pp. 2091-2101 ◽  
Author(s):  
M. S. Sandhu ◽  
D. M. Baekey ◽  
N. G. Maling ◽  
J. C. Sanchez ◽  
P. J. Reier ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Phrenic Nerve ◽  
Discharge Rate ◽  
Nerve Activity ◽  
Adult Rats ◽  
Phrenic Nerve Activity ◽  
Monosynaptic Connection ◽  
Nerve Signal ◽  
Phrenic Motoneurons ◽  
Discharge Patterns

Anatomical evidence indicates that midcervical interneurons can be synaptically coupled with phrenic motoneurons. Accordingly, we hypothesized that interneurons in the C3–C4 spinal cord can display discharge patterns temporally linked with inspiratory phrenic motor output. Anesthetized adult rats were studied before, during, and after a 4-min bout of moderate hypoxia. Neuronal discharge in C3–C4 lamina I–IX was monitored using a multielectrode array while phrenic nerve activity was extracellularly recorded. For the majority of cells, spike-triggered averaging (STA) of ipsilateral inspiratory phrenic nerve activity based on neuronal discharge provided no evidence of discharge synchrony. However, a distinct STA phrenic peak with a 6.83 ± 1.1 ms lag was present for 5% of neurons, a result that indicates a monosynaptic connection with phrenic motoneurons. The majority (93%) of neurons changed discharge rate during hypoxia, and the diverse responses included both increased and decreased firing. Hypoxia did not change the incidence of STA peaks in the phrenic nerve signal. Following hypoxia, 40% of neurons continued to discharge at rates above prehypoxia values (i.e., short-term potentiation, STP), and cells with initially low discharge rates were more likely to show STP ( P < 0.001). We conclude that a population of nonphrenic C3–C4 neurons in the rat spinal cord is synaptically coupled to the phrenic motoneuron pool, and these cells can modulate inspiratory phrenic output. In addition, the C3–C4 propriospinal network shows a robust and complex pattern of activation both during and following an acute bout of hypoxia.

Inspiratory rhythm in airway smooth muscle tone

1985 ◽  
Vol 58 (3) ◽  
pp. 911-920 ◽  
Author(s):  
R. A. Mitchell ◽  
D. A. Herbert ◽  
D. G. Baker
Keyword(s):  
Smooth Muscle ◽  
Vagus Nerve ◽  
Airway Smooth Muscle ◽  
Phrenic Nerve ◽  
Nerve Activity ◽  
Lung Inflation ◽  
Phrenic Nerve Activity ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Stimulation Of

In anesthetized paralyzed open-chested cats ventilated with low tidal volumes at high frequency, we recorded phrenic nerve activity, transpulmonary pressure (TPP), and either the tension in an upper tracheal segment or the impulse activity in a pulmonary branch of the vagus nerve. The TPP and upper tracheal segment tension fluctuated with respiration, with peak pressure and tension paralleling phrenic nerve activity. Increased end-tidal CO2 or stimulation of the carotid chemoreceptors with sodium cyanide increased both TPP and tracheal segment tension during the increased activity of the phrenic nerve. Lowering end-tidal CO2 or hyperinflating the lungs to achieve neural apnea (lack of phrenic activity) caused a decrease in TPP and tracheal segment tension and abolished the inspiratory fluctuations. During neural apnea produced by lowering end-tidal CO2, lung inflation caused no further decrease in tracheal segment tension and TPP. Likewise, stimulation of the cervical sympathetics, which caused a reduction in TPP and tracheal segment tension during normal breathing, caused no further reduction in these parameters when the stimulation occurred during neural apnea. During neural apnea the tracheal segment tension and TPP were the same as those following the transection of the vagi or the administration of atropine (0.5 mg/kg). Numerous fibers in the pulmonary branch of the vagus nerve fired in synchrony with the phrenic nerve. Only these fibers had activity which paralleled changes in TPP and tracheal tension. We propose that the major excitatory input to airway smooth muscle arises from cholinergic nerves that fire during inspiration, which have preganglionic cell bodies in the ventral respiratory group in the region of the nucleus ambiguus and are driven by the same pattern generators that drive the phrenic and inspiratory intercostal motoneurons.

Basis for late expiratory spinal inhibition of phrenic nerve discharge

1975 ◽  
Vol 228 (6) ◽  
pp. 1690-1694 ◽  
Author(s):  
AT Zielinski ◽  
GL Gebber
Keyword(s):  
Phrenic Nerve ◽  
Superior Laryngeal Nerve ◽  
Intercostal Nerve ◽  
Nerve Activity ◽  
Nerve Response ◽  
The Relationship ◽  
Decerebrate Cats ◽  
Spinal Inhibition ◽  
Stimulation Of ◽  
Nerve Discharge

The relationship between spinal inhibition of phrenic nerve activity and thoratic expiratory motoneuronal discharge was studied in chloralose-anesthetized and unanesthetized decerebrate cats. The amplitude of the phrenic nerve response elicited by singleshocks applied to descending tracts in the second cervical spinal segment progressively fell during the late expiratory phase of the central respiratory cycle. The depression resulted, at least in part, from active spinal inhibition since the spina-to-phrenic evoked response was smaller in late expiration than after C'1 spinal transection. Inhibition of the spinal-to-phrenic evoked was time-locked to the spontaneousburst of activity recorded from the eigth internal intercostal nerve. The degree of inhibition of the spinal-to-phenic evoked discharge was directly related to theamplitude of spontaneously occurring internal intercostal nerve activity. A similiarrelationship was observed when internal intercostal nerve activity and spinal inhibitionof phrenic discharge were evoked by stimulation of the superior laryngeal nerve. It is concluded htat late expiratory spinal inhibition of phrenic discharge was dependent on those neural events responsible for the activation of thoracic expiratory motoneurons.

Altered breathing pattern elicited by stimulation of abdominal visceral afferents

1985 ◽  
Vol 58 (6) ◽  
pp. 1755-1760 ◽  
Author(s):  
N. R. Prabhakar ◽  
W. Marek ◽  
H. H. Loeschcke
Keyword(s):  
Small Intestine ◽  
Phrenic Nerve ◽  
Muscle Activity ◽  
Breathing Pattern ◽  
Recovery Phase ◽  
Visceral Afferents ◽  
Intercostal Muscle ◽  
Nerve Activity ◽  
Phrenic Nerve Activity ◽  
Stimulation Of

The effect of stimulation of afferent mesenteric nerves on tidal volume (VT), phrenic nerve, and external intercostal muscle activities was studied in anesthetized spontaneously breathing cats. Both mechanical distension of the small intestine and electrical stimulation of the mesenteric nerves resulted in an initial inspiratory inhibition of VT followed by a gradual recovery above the prestimulus controls. Changes in VT were accompanied by a depression of phrenic nerve activity and an excitation of external intercostal muscle activity. During the recovery phase of VT, the amplitude of phrenic nerve activity returned only partially, whereas the activity of the external intercostal muscle was greater than the prestimulus controls. In a second group of experiments, brief tetanic stimulation at the beginning of inspiration led to a complete and maintained inhibition of phrenic nerve activity but with a simultaneous excitation of external intercostal muscle activity and without any change in VT; whereas expiratory stimulation caused a decrease in expiratory abdominal muscle activity, without changing the peak amplitude of phrenic nerve activity. The respiratory changes observed with distension of the small intestine were abolished after denervation of the mesenteric plexus. It is concluded that activation of the visceral afferents of the mesenteric region reflexly changes diaphragmatic breathing to intercostal breathing. It is assumed that such a type of breathing pattern may occur in pregnancy and in pathophysiological situations involving splanchnic viscera.

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