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Evidence for TREK‐like Tandem Pore Domain Channels in Intrapulmonary Chemoreceptor Chemotransduction
Author(s) -
Bina Robert Wagner,
Hempleman Steven
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a787-a
Subject(s) - isoflurane , halothane , acidosis , potassium channel , chemistry , inhalation , extracellular , diethyl ether , anesthesia , chemoreceptor , depolarization , minimum alveolar concentration , biophysics , medicine , biochemistry , biology , receptor , chromatography
Intrapulmonary chemoreceptors (IPC) are CO2‐sensing neurons which innervate the lungs of birds, control breathing pattern, and are inhibited by halothane and intracellular acidosis. Recently, a novel class of potassium background leak channels has been characterized, the tandem pore domain channels, that are important in setting the resting membrane potential from which neurons depolarize to conduct action potentials. Some of these channels, including the TASK and TREK families, are activated by volatile anesthetics and acidosis. We hypothesized that such channels might underlie signal transduction in IPC. We treated 24 mallard ducks of both sexes with inspired isoflurane, halothane, chloroform, and diethyl ether in increasing concentrations, to test their effects on the frequency of IPC discharge through single cell, extracellular recording from vagal fibers. Isoflurane inhalation had no effect on IPC discharge at treatment levels less than 9%, which depressed peak IPC discharge by 53% (p<0.0001). Halothane at 1%, 2%, 4%, 6%, and 9% attenuated IPC peak discharge by 24.9%, 26.6%, 50.9%, 30.9%, and 37.8%, respectively (p<0.0001). Chloroform at 4%, 6%, and 9% depressed IPC peak discharge by 34.3%, 62.9% and 69.7%, respectively (p<0.0001). Ether at 2%, 3%, and 4% greatly attenuated IPC peak discharge by 60.5%, 93.8%, and 96.6%, respectively (p<0.0001). Greater IPC inhibition by ether, chloroform, and halothane compared to isoflurane suggest that IPC express tandem‐pore domain leak channels most similar to the TREK (rather than TASK) family. TREK channel expression also explains known IPC sensitivity to intracellular acidosis. Support: NSF 0217815