Expression and characterization of delayed rectifying K+ channels in anterior rat taste buds

1 Department of Biology and The Center for Integrated BioSystems, Utah State University, Logan, Utah; 2 Brain Research Centre, University of British Columbia, Vancouver, British Columbia, Canada; and 3 Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas Submitted 11 March 2005 ; accepted in final form 20 May 2005 Delayed rectifying K + (DRK) channels in taste cells have been implicated in the regulation of cell excitability and as potential targets for direct and indirect modulation by taste stimuli. In the present study, we have used patch-clamp recording to determine the biophysical properties and pharmacological sensitivity of DRK channels in isolated rat fungiform taste buds. Molecular biological assays at the taste bud and single-cell levels are consistent with the interpretation that taste cells express a variety of DRK channels, including members from each of the three major subfamilies: KCNA, KCNB, and KCNC. Real-time PCR assays were used to quantify expression of the nine DRK channel subtypes. While taste cells express a number of DRK channels, the electrophysiological and molecular biological assays indicate that the Shaker Kv1.5 channel (KCNA5) is the major functional DRK channel expressed in the anterior rat tongue. transduction Address for reprint requests and other correspondence: T. A. Gilbertson, Dept. of Biology, Utah State Univ., 5305 Old Main Hill, Logan, UT 84322-5305 (e-mail: tag{at}biology.usu.edu )