Acid-Sensitive Two-Pore Domain Potassium (K2P) Channels in Mouse Taste Buds
1 Department of Physiology and Biophysics, and 2 Neuroscience Program, University of Miami School of Medicine, Miami, Florida 33136 Submitted 19 March 2004; accepted in final form 7 May 2004 Sour (acid) taste is postulated to result from intracellular acidification that modulates one or more acid-se...
Gespeichert in:
Veröffentlicht in: | Journal of neurophysiology 2004-09, Vol.92 (3), p.1928-1936 |
---|---|
Hauptverfasser: | , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | 1 Department of Physiology and Biophysics, and 2 Neuroscience Program, University of Miami School of Medicine, Miami, Florida 33136
Submitted 19 March 2004;
accepted in final form 7 May 2004
Sour (acid) taste is postulated to result from intracellular acidification that modulates one or more acid-sensitive ion channels in taste receptor cells. The identity of such channel(s) remains uncertain. Potassium channels, by regulating the excitability of taste cells, are candidates for acid transducers. Several 2-pore domain potassium leak conductance channels (K 2 P family) are sensitive to intracellular acidification. We examined their expression in mouse vallate and foliate taste buds using RT-PCR, and detected TWIK-1 and -2, TREK-1 and -2, and TASK-1. Of these, TWIK-1 and TASK-1 were preferentially expressed in taste cells relative to surrounding nonsensory epithelium. The related TRESK channel was not detected, whereas the acid-insensitive TASK-2 was. Using confocal imaging with pH-, Ca 2+ -, and voltage-sensitive dyes, we tested pharmacological agents that are diagnostic for these channels. Riluzole (500 µM), selective for TREK-1 and -2 channels, enhanced acid taste responses. In contrast, halothane ( 17 mM), which acts on TREK-1 and TASK-1 channels, blocked acid taste responses. Agents diagnostic for other 2-pore domain and voltage-gated potassium channels (anandamide, 10 µM; Gd 3+ , 1 mM; arachidonic acid, 100 µM; quinidine, 200 µM; quinine, 100 mM; 4-AP, 10 mM; and TEA, 1 mM) did not affect acid responses. The expression of 2-pore domain channels and our pharmacological characterization suggest that a matrix of ion channels, including one or more acid-sensitive 2-pore domain K channels, could play a role in sour taste transduction. However, our results do not unambiguously identify any one channel as the acid taste transducer.
Address for reprint requests and other correspondence: S. Roper, Dept. of Physiology and Biophysics, University of Miami School of Medicine, 1600 NW 10th Ave., Miami, FL 33136 (E-mail: Roper{at}miami.edu ). |
---|---|
ISSN: | 0022-3077 1522-1598 |
DOI: | 10.1152/jn.00273.2004 |