Evidence for TREK-like tandem-pore domain channels in intrapulmonary chemoreceptor chemotransduction

Robert Wagner Bina, Steven C Hempleman

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Intrapulmonary chemoreceptors (IPC) are carbon dioxide sensing neurons that innervate the lungs of birds, control breathing pattern, and are inhibited by halothane and intracellular acidosis. TASK and TREK are subfamilies of tandem-pore domain potassium leak channels, important in setting resting membrane potential, that are affected by volatile anesthetics and acidosis. We hypothesized that such channels might underlie signal transduction in IPC. We treated mallard ducks with four volatile anesthetics in increasing concentrations to test their effects on IPC discharge through single cell, extracellular recording from vagal fibers. Isoflurane inhalation attenuated IPC discharge only at 8.25% inspired (α = 0.05). Halothane attenuated IPC discharge significantly (α = 0.05) at all treatment levels. Chloroform at 3.8%, 5.6%, and 8.25% significantly attenuated IPC discharge (α = 0.05). Ether at 1.9%, 2.9%, and 3.8% significantly attenuated IPC discharge (α = 0.05), abolishing IPC discharge at 3.8% inspired. The pharmacological signature of IPC discharge attenuation suggests that IPC express tandem-pore domain leak channels similar to TREK channels, which are inhibited by intracellular acidosis.

Original languageEnglish (US)
Pages (from-to)120-131
Number of pages12
JournalRespiratory Physiology and Neurobiology
Volume156
Issue number2
DOIs
StatePublished - May 14 2007

Fingerprint

Acidosis
Halothane
Tandem Pore Domain Potassium Channels
Anesthetics
Ducks
Isoflurane
Chloroform
Carbon Dioxide
Ether
Membrane Potentials
Inhalation
Birds
Signal Transduction
Respiration
Pharmacology
Neurons
Lung

Keywords

  • Carbon dioxide
  • Control of breathing
  • Potassium leak channels
  • Signal transduction
  • Volatile anesthesics

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Neuroscience(all)

Cite this

Evidence for TREK-like tandem-pore domain channels in intrapulmonary chemoreceptor chemotransduction. / Bina, Robert Wagner; Hempleman, Steven C.

In: Respiratory Physiology and Neurobiology, Vol. 156, No. 2, 14.05.2007, p. 120-131.

Research output: Contribution to journalArticle

@article{2ea4ca0386c748f1a0249011e37bdb00,
title = "Evidence for TREK-like tandem-pore domain channels in intrapulmonary chemoreceptor chemotransduction",
abstract = "Intrapulmonary chemoreceptors (IPC) are carbon dioxide sensing neurons that innervate the lungs of birds, control breathing pattern, and are inhibited by halothane and intracellular acidosis. TASK and TREK are subfamilies of tandem-pore domain potassium leak channels, important in setting resting membrane potential, that are affected by volatile anesthetics and acidosis. We hypothesized that such channels might underlie signal transduction in IPC. We treated mallard ducks with four volatile anesthetics in increasing concentrations to test their effects on IPC discharge through single cell, extracellular recording from vagal fibers. Isoflurane inhalation attenuated IPC discharge only at 8.25{\%} inspired (α = 0.05). Halothane attenuated IPC discharge significantly (α = 0.05) at all treatment levels. Chloroform at 3.8{\%}, 5.6{\%}, and 8.25{\%} significantly attenuated IPC discharge (α = 0.05). Ether at 1.9{\%}, 2.9{\%}, and 3.8{\%} significantly attenuated IPC discharge (α = 0.05), abolishing IPC discharge at 3.8{\%} inspired. The pharmacological signature of IPC discharge attenuation suggests that IPC express tandem-pore domain leak channels similar to TREK channels, which are inhibited by intracellular acidosis.",
keywords = "Carbon dioxide, Control of breathing, Potassium leak channels, Signal transduction, Volatile anesthesics",
author = "Bina, {Robert Wagner} and Hempleman, {Steven C}",
year = "2007",
month = "5",
day = "14",
doi = "10.1016/j.resp.2006.09.005",
language = "English (US)",
volume = "156",
pages = "120--131",
journal = "Respiratory Physiology and Neurobiology",
issn = "1569-9048",
publisher = "Elsevier",
number = "2",

}

TY - JOUR

T1 - Evidence for TREK-like tandem-pore domain channels in intrapulmonary chemoreceptor chemotransduction

AU - Bina, Robert Wagner

AU - Hempleman, Steven C

PY - 2007/5/14

Y1 - 2007/5/14

N2 - Intrapulmonary chemoreceptors (IPC) are carbon dioxide sensing neurons that innervate the lungs of birds, control breathing pattern, and are inhibited by halothane and intracellular acidosis. TASK and TREK are subfamilies of tandem-pore domain potassium leak channels, important in setting resting membrane potential, that are affected by volatile anesthetics and acidosis. We hypothesized that such channels might underlie signal transduction in IPC. We treated mallard ducks with four volatile anesthetics in increasing concentrations to test their effects on IPC discharge through single cell, extracellular recording from vagal fibers. Isoflurane inhalation attenuated IPC discharge only at 8.25% inspired (α = 0.05). Halothane attenuated IPC discharge significantly (α = 0.05) at all treatment levels. Chloroform at 3.8%, 5.6%, and 8.25% significantly attenuated IPC discharge (α = 0.05). Ether at 1.9%, 2.9%, and 3.8% significantly attenuated IPC discharge (α = 0.05), abolishing IPC discharge at 3.8% inspired. The pharmacological signature of IPC discharge attenuation suggests that IPC express tandem-pore domain leak channels similar to TREK channels, which are inhibited by intracellular acidosis.

AB - Intrapulmonary chemoreceptors (IPC) are carbon dioxide sensing neurons that innervate the lungs of birds, control breathing pattern, and are inhibited by halothane and intracellular acidosis. TASK and TREK are subfamilies of tandem-pore domain potassium leak channels, important in setting resting membrane potential, that are affected by volatile anesthetics and acidosis. We hypothesized that such channels might underlie signal transduction in IPC. We treated mallard ducks with four volatile anesthetics in increasing concentrations to test their effects on IPC discharge through single cell, extracellular recording from vagal fibers. Isoflurane inhalation attenuated IPC discharge only at 8.25% inspired (α = 0.05). Halothane attenuated IPC discharge significantly (α = 0.05) at all treatment levels. Chloroform at 3.8%, 5.6%, and 8.25% significantly attenuated IPC discharge (α = 0.05). Ether at 1.9%, 2.9%, and 3.8% significantly attenuated IPC discharge (α = 0.05), abolishing IPC discharge at 3.8% inspired. The pharmacological signature of IPC discharge attenuation suggests that IPC express tandem-pore domain leak channels similar to TREK channels, which are inhibited by intracellular acidosis.

KW - Carbon dioxide

KW - Control of breathing

KW - Potassium leak channels

KW - Signal transduction

KW - Volatile anesthesics

UR - http://www.scopus.com/inward/record.url?scp=33847415528&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33847415528&partnerID=8YFLogxK

U2 - 10.1016/j.resp.2006.09.005

DO - 10.1016/j.resp.2006.09.005

M3 - Article

VL - 156

SP - 120

EP - 131

JO - Respiratory Physiology and Neurobiology

JF - Respiratory Physiology and Neurobiology

SN - 1569-9048

IS - 2

ER -