Excitation of dorsal and ventral respiratory group neurons by phrenic nerve afferents

The projections of phrenic nerve afferents to neurons in the dorsal (DRG) and ventral (VRG) respiratory group were studied in anesthetized, paralyzed, and vagotomized cats. Extracellular recordings of neuronal responses to vagal nerve and cervical phrenic nerve stimulation (CPNS) indicated that about one-fourth of the DRG respiratory-modulated neurons were excited by phrenic nerve afferents with an onset latency of approximately 20 ms. In addition, non-respiratory-modulated neurons within the DRG were recruited by CPNS. Although some convergence of vagal and phrenic afferent input was observed, most neurons were affected by only one type of afferent. In contrast to the DRG, only 3 out of 28 VRG respiratory-modulated neurons responded to CPNS. A second study determined that most of these neuronal responses were due to activation of diaphragmatic afferents since 90% of the DRG units activated by CPNS were also excited at a longer latency by thoracic phrenic nerve stimulation. The difference in onset latency of neuronal excitation indicates an afferent peripheral conduction velocity of about 10 m/s, which suggests that they are predominately small myelinated fibers (group III) making paucisynaptic connections with DRG neurons. Decerebration, decerebellation, and bilateral transection of the dorsal columns at C2 do not abolish the neuronal responses to cervical PNS.

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Attenuation of phrenic motor discharge by phrenic nerve afferents

Journal of Applied Physiology ◽

10.1152/jappl.1987.62.3.941 ◽

1987 ◽

Vol 62 (3) ◽

pp. 941-945 ◽

Cited By ~ 40

Author(s):

D. F. Speck ◽

W. R. Revelette

Keyword(s):

Nerve Stimulation ◽

Phrenic Nerve ◽

Short Latency ◽

Onset Latency ◽

Phrenic Nerve Stimulation ◽

Group Iii ◽

Dorsal Columns ◽

The Difference ◽

Contralateral Response ◽

The Right

Short latency phrenic motor responses to phrenic nerve stimulation were studied in anesthetized, paralyzed cats. Electrical stimulation (0.2 ms, 0.01–10 mA, 2 Hz) of the right C5 phrenic rootlet during inspiration consistently elicited a transient reduction in the phrenic motor discharge. This attenuation occurred bilaterally with an onset latency of 8–12 ms and a duration of 8–30 ms. Section of the ipsilateral C4-C6 dorsal roots abolished the response to stimulation, thereby confirming the involvement of phrenic nerve afferent activity. Stimulation of the left C5 phrenic rootlet or the right thoracic phrenic nerve usually elicited similar inhibitory responses. The difference in onset latency of responses to cervical vs. thoracic phrenic nerve stimulation indicates activation of group III afferents with a peripheral conduction velocity of approximately 10 m/s. A much shorter latency response (5 ms) was evoked ipsilaterally by thoracic phrenic nerve stimulation. Section of either the C5 or C6 dorsal root altered the ipsilateral response so that it resembled the longer latency contralateral response. The low-stimulus threshold and short latency for the ipsilateral response to thoracic phrenic nerve stimulation suggest that it involves larger diameter fibers. Decerebration, decerebellation, and transection of the dorsal columns at C2 do not abolish the inhibitory phrenic-to-phrenic reflex.

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The effect of diaphragm contraction on upper airway collapsibility

Journal of Applied Physiology ◽

10.1152/japplphysiol.01199.2012 ◽

2013 ◽

Vol 115 (3) ◽

pp. 337-345 ◽

Cited By ~ 6

Author(s):

David R. Hillman ◽

Jennifer H. Walsh ◽

Kathleen J. Maddison ◽

Peter R. Platt ◽

Alan R. Schwartz ◽

...

Keyword(s):

Nerve Stimulation ◽

Lung Volume ◽

Phrenic Nerve ◽

Upper Airway ◽

Dependent Manner ◽

Phrenic Nerve Stimulation ◽

Airway Patency ◽

Airway Collapsibility ◽

The Difference ◽

Upper Airway Collapsibility

Increasing lung volume increases upper airway patency and decreases airway resistance and collapsibility. The role of diaphragm contraction in producing these changes remains unclear. This study was undertaken to determine the effect of selective diaphragm contraction, induced by phrenic nerve stimulation, on upper airway collapsibility and the extent to which any observed change was attributable to lung volume-related changes in pressure gradients or to diaphragm descent-related mediastinal traction. Continuous bilateral transcutaneous cervical phrenic nerve stimulation (30 Hz) was applied to nine supine, anesthetized human subjects during transient decreases in airway pressure to levels sufficient to produce flow limitation when unstimulated. Stimulation was applied at two intensities (low and high) and its effects on lung volume and airflow quantified relative to unstimulated conditions. Lung volume increased by 386 ± 269 ml (means ± SD) and 761 ± 556 ml during low and high stimulation, respectively ( P < 0.05 for the difference between these values), which was associated with peak inspiratory flow increases of 69 ± 57 and 137 ± 108 ml/s, respectively ( P < 0.05 for the difference). Stimulation-induced change in lung volume correlated with change in peak flow ( r = 0.65, P < 0.01). Diaphragm descent-related outward displacement of the abdominal wall produced no change in airflow unless accompanied by lung volume change. We conclude that phrenic nerve stimulation-induced diaphragm contraction increases lung volume and reduces airway collapsibility in a dose-dependent manner. The effect appears primarily mediated by changes in lung volume rather than mediastinal traction from diaphragm descent. The study provides a rationale for use of continuous phrenic stimulation to treat obstructive sleep apnea.

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Relative contribution of neurotransmission failure to diaphragm fatigue

Journal of Applied Physiology ◽

10.1152/jappl.1990.68.1.174 ◽

1990 ◽

Vol 68 (1) ◽

pp. 174-180 ◽

Cited By ~ 42

Author(s):

J. H. Kuei ◽

R. Shadmehr ◽

G. C. Sieck

Keyword(s):

Nerve Stimulation ◽

Phrenic Nerve ◽

Neural Stimulation ◽

Muscle Stimulation ◽

Phrenic Nerve Stimulation ◽

Relative Contribution ◽

The Difference ◽

Second Procedure ◽

Phrenic Stimulation ◽

Diaphragm Fatigue

Two procedures were used to estimate the relative contribution of neurotransmission failure (NF) to fatigue of the rat diaphragm at different rates of phrenic nerve stimulation. In one, direct muscle stimulation was intermittently superimposed on neural stimulation of the diaphragm, and the relative contribution of NF was estimated by the difference in generated tension. In a second procedure, diaphragm fatigue was induced by using either direct muscle stimulation (with complete blockade of the neuromuscular junction by d-tubocurare) or phrenic nerve stimulation. The relative contribution of NF to diaphragm fatigue was then estimated by comparing the force loss during these two modes of stimulation. With both procedures, it was observed that 1) the relative contribution of NF to diaphragm fatigue was less than 45% at each frequency of phrenic nerve stimulation; 2) the relative contribution of NF to diaphragm fatigue increased at higher rates of phrenic stimulation, reaching a maximum at 75 pulses/s; and 3) the relative contribution of NF to diaphragm fatigue reached a plateau after 2 min of repetitive stimulation.

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Botzinger complex region role in phrenic-to-phrenic inhibitory reflex of cat

Journal of Applied Physiology ◽

10.1152/jappl.1989.67.4.1364 ◽

1989 ◽

Vol 67 (4) ◽

pp. 1364-1370 ◽

Cited By ~ 12

Author(s):

D. F. Speck

Keyword(s):

Nerve Stimulation ◽

Phrenic Nerve ◽

Inhibitory Response ◽

Phrenic Nerve Stimulation ◽

Bötzinger Complex ◽

Before And After ◽

Pass Through ◽

Bilateral Lesions ◽

Decerebrate Cats ◽

Inhibitory Reflex

Neuronal recordings, microstimulation, and electrolytic and chemical lesions were used to examine the involvement of the Botzinger Complex (BotC) in the bilateral phrenic-to-phrenic inhibitory reflex. Experiments were conducted in decerebrate cats that were paralyzed, ventilated, thoracotomized, and vagotomized. Microelectrode recordings within the BotC region revealed that some neurons were activated by phrenic nerve stimulation (15 of 69 expiratory units, 9 of 67 inspiratory units, and 19 nonrespiratory-modulated units) at average latencies similar to the onset latency of the phrenic-to-phrenic inhibition. In addition, microstimulation within the BotC caused a short latency transient inhibition of phrenic motor activity. In 17 cats phrenic neurogram responses to threshold and supramaximal (15 mA) stimulation of phrenic nerve afferents were recorded before and after electrolytic BotC lesions. In 15 animals the inhibitory reflex was attenuated by bilateral lesions. Because lesion of either BotC neurons or axons of passage could account for this attenuation, in eight experiments the phrenic-to-phrenic inhibitory responses were recorded before and after bilateral injections of 5 microM kainic acid (30–150 nl) into the BotC. After chemical lesions, the inhibitory response to phrenic nerve stimulation remained; however, neuronal activity typical of the BotC could not be located. These results suggest that axons important in producing the phrenic-to-phrenic reflex pass through the region of the BotC, but that BotC neurons themselves are not necessary for this reflex.

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