Pulmonary C-fiber receptor activation abolishes uncoupled facial nerve activity from phrenic bursting during positive end-expired pressure in the rat

Kun Ze Lee, David D. Fuller, I. Jung Lu, Li Chi Ku, Ji Chuu Hwang

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Phasic respiratory bursting in the facial nerve (FN) can be uncoupled from phrenic bursting by application of 9 cmH2O positive end-expired pressure (PEEP). This response reflects excitation of expiratory-inspiratory (EI) and preinspiratory (Pre-I) facial neurons during the Pre-I period and inhibition of EI neurons during inspiration (I). Because activation of pulmonary C-fiber (PCF) receptors can inhibit the discharge of EI and Pre-I neurons, we hypothesized that PCF receptor activation via capsaicin would attenuate or abolish uncoupled FN bursting with an increase from 3 cmH2O (baseline) to 9 cmH2O PEEP. Neurograms were recorded in the FN and phrenic nerve in anesthetized, ventilated, vagally intact adult Wistar rats. Increasing PEEP to 9 cmH2O resulted in a persistent rhythmic discharge in the FN during phrenic quiescence (i.e., uncoupled bursting). Combination of PEEP with intrajugular capsaicin injection severely attenuated or eliminated uncoupled bursting in the FN (P < 0.05). Additional experiments examined the pattern of facial motoneuron (vs. neurogram) bursting during PEEP application and capsaicin treatment. These single-fiber recordings confirmed that Pre-I and EI (but not I) neurons continued to burst during PEEP-induced phrenic apnea. Capsaicin treatment during PEEP substantially inhibited Pre-I and EI neuron discharge. Finally, analyses of FN and motoneuron bursting across the respiratory cycle indicated that the inhibitory effects of capsaicin were more pronounced during the Pre-I period. We conclude that activation of PCF receptors can inhibit FN bursting during PEEP-induced phrenic apnea by inhibiting EI and I facial motoneuron discharge.

Original languageEnglish
Pages (from-to)119-129
Number of pages11
JournalJournal of Applied Physiology
Volume104
Issue number1
DOIs
Publication statusPublished - 2008 Jan 1

Fingerprint

Unmyelinated Nerve Fibers
Facial Nerve
Diaphragm
Capsaicin
Pressure
Lung
Neurons
Motor Neurons
Apnea
Phrenic Nerve
Wistar Rats
Injections
Therapeutics

Keywords

  • Facial motoneurons
  • Pulmonary stretch receptors

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Pulmonary C-fiber receptor activation abolishes uncoupled facial nerve activity from phrenic bursting during positive end-expired pressure in the rat. / Lee, Kun Ze; Fuller, David D.; Lu, I. Jung; Ku, Li Chi; Hwang, Ji Chuu.

In: Journal of Applied Physiology, Vol. 104, No. 1, 01.01.2008, p. 119-129.

Research output: Contribution to journalArticle

@article{d1964bba86074d18890a96b8a1bcd274,
title = "Pulmonary C-fiber receptor activation abolishes uncoupled facial nerve activity from phrenic bursting during positive end-expired pressure in the rat",
abstract = "Phasic respiratory bursting in the facial nerve (FN) can be uncoupled from phrenic bursting by application of 9 cmH2O positive end-expired pressure (PEEP). This response reflects excitation of expiratory-inspiratory (EI) and preinspiratory (Pre-I) facial neurons during the Pre-I period and inhibition of EI neurons during inspiration (I). Because activation of pulmonary C-fiber (PCF) receptors can inhibit the discharge of EI and Pre-I neurons, we hypothesized that PCF receptor activation via capsaicin would attenuate or abolish uncoupled FN bursting with an increase from 3 cmH2O (baseline) to 9 cmH2O PEEP. Neurograms were recorded in the FN and phrenic nerve in anesthetized, ventilated, vagally intact adult Wistar rats. Increasing PEEP to 9 cmH2O resulted in a persistent rhythmic discharge in the FN during phrenic quiescence (i.e., uncoupled bursting). Combination of PEEP with intrajugular capsaicin injection severely attenuated or eliminated uncoupled bursting in the FN (P < 0.05). Additional experiments examined the pattern of facial motoneuron (vs. neurogram) bursting during PEEP application and capsaicin treatment. These single-fiber recordings confirmed that Pre-I and EI (but not I) neurons continued to burst during PEEP-induced phrenic apnea. Capsaicin treatment during PEEP substantially inhibited Pre-I and EI neuron discharge. Finally, analyses of FN and motoneuron bursting across the respiratory cycle indicated that the inhibitory effects of capsaicin were more pronounced during the Pre-I period. We conclude that activation of PCF receptors can inhibit FN bursting during PEEP-induced phrenic apnea by inhibiting EI and I facial motoneuron discharge.",
keywords = "Facial motoneurons, Pulmonary stretch receptors",
author = "Lee, {Kun Ze} and Fuller, {David D.} and Lu, {I. Jung} and Ku, {Li Chi} and Hwang, {Ji Chuu}",
year = "2008",
month = "1",
day = "1",
doi = "10.1152/japplphysiol.00505.2007",
language = "English",
volume = "104",
pages = "119--129",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "1",

}

TY - JOUR

T1 - Pulmonary C-fiber receptor activation abolishes uncoupled facial nerve activity from phrenic bursting during positive end-expired pressure in the rat

AU - Lee, Kun Ze

AU - Fuller, David D.

AU - Lu, I. Jung

AU - Ku, Li Chi

AU - Hwang, Ji Chuu

PY - 2008/1/1

Y1 - 2008/1/1

N2 - Phasic respiratory bursting in the facial nerve (FN) can be uncoupled from phrenic bursting by application of 9 cmH2O positive end-expired pressure (PEEP). This response reflects excitation of expiratory-inspiratory (EI) and preinspiratory (Pre-I) facial neurons during the Pre-I period and inhibition of EI neurons during inspiration (I). Because activation of pulmonary C-fiber (PCF) receptors can inhibit the discharge of EI and Pre-I neurons, we hypothesized that PCF receptor activation via capsaicin would attenuate or abolish uncoupled FN bursting with an increase from 3 cmH2O (baseline) to 9 cmH2O PEEP. Neurograms were recorded in the FN and phrenic nerve in anesthetized, ventilated, vagally intact adult Wistar rats. Increasing PEEP to 9 cmH2O resulted in a persistent rhythmic discharge in the FN during phrenic quiescence (i.e., uncoupled bursting). Combination of PEEP with intrajugular capsaicin injection severely attenuated or eliminated uncoupled bursting in the FN (P < 0.05). Additional experiments examined the pattern of facial motoneuron (vs. neurogram) bursting during PEEP application and capsaicin treatment. These single-fiber recordings confirmed that Pre-I and EI (but not I) neurons continued to burst during PEEP-induced phrenic apnea. Capsaicin treatment during PEEP substantially inhibited Pre-I and EI neuron discharge. Finally, analyses of FN and motoneuron bursting across the respiratory cycle indicated that the inhibitory effects of capsaicin were more pronounced during the Pre-I period. We conclude that activation of PCF receptors can inhibit FN bursting during PEEP-induced phrenic apnea by inhibiting EI and I facial motoneuron discharge.

AB - Phasic respiratory bursting in the facial nerve (FN) can be uncoupled from phrenic bursting by application of 9 cmH2O positive end-expired pressure (PEEP). This response reflects excitation of expiratory-inspiratory (EI) and preinspiratory (Pre-I) facial neurons during the Pre-I period and inhibition of EI neurons during inspiration (I). Because activation of pulmonary C-fiber (PCF) receptors can inhibit the discharge of EI and Pre-I neurons, we hypothesized that PCF receptor activation via capsaicin would attenuate or abolish uncoupled FN bursting with an increase from 3 cmH2O (baseline) to 9 cmH2O PEEP. Neurograms were recorded in the FN and phrenic nerve in anesthetized, ventilated, vagally intact adult Wistar rats. Increasing PEEP to 9 cmH2O resulted in a persistent rhythmic discharge in the FN during phrenic quiescence (i.e., uncoupled bursting). Combination of PEEP with intrajugular capsaicin injection severely attenuated or eliminated uncoupled bursting in the FN (P < 0.05). Additional experiments examined the pattern of facial motoneuron (vs. neurogram) bursting during PEEP application and capsaicin treatment. These single-fiber recordings confirmed that Pre-I and EI (but not I) neurons continued to burst during PEEP-induced phrenic apnea. Capsaicin treatment during PEEP substantially inhibited Pre-I and EI neuron discharge. Finally, analyses of FN and motoneuron bursting across the respiratory cycle indicated that the inhibitory effects of capsaicin were more pronounced during the Pre-I period. We conclude that activation of PCF receptors can inhibit FN bursting during PEEP-induced phrenic apnea by inhibiting EI and I facial motoneuron discharge.

KW - Facial motoneurons

KW - Pulmonary stretch receptors

UR - http://www.scopus.com/inward/record.url?scp=38348999106&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=38348999106&partnerID=8YFLogxK

U2 - 10.1152/japplphysiol.00505.2007

DO - 10.1152/japplphysiol.00505.2007

M3 - Article

C2 - 17916674

AN - SCOPUS:38348999106

VL - 104

SP - 119

EP - 129

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 1

ER -