title: Ca(2+)-activated nonselective cation, maxi K+ and Cl- channels in apical membrane of marginal cells of stria vascularis.
abstract: Patch clamp recordings on the apical membrane of marginal cells of the stria vascularis of the gerbil were made in the cell-attached and excised configuration. Marginal cells are thought to secrete K+ into and absorb Na+ from endolymph. Four types of channel were identified; the most frequently observed channel was a small, nonselective cation channel which was highly similar to that found in the apical membrane of vestibular dark cells (Marcus et al., (1992) Am. J. Physiol. 262, C1423-C1429). The small nonselective cation channel was equally conductive (26.7 +/- 0.3 pS; N = 49) for K+, Na+, Rb+, Li+ and Cs+, 1.6 times more permeable to NH4+, but not permeable to Cl-, Ca2+, Ba2+ or N-methyl-D-glucamine. This channel yielded linear current-voltage relations which passed nearly through the origin (intercept: -2.2 +/- 0.4 mV, N = 49) when conductive monovalent cations were present on both sides of the membrane in equal concentrations. Channel activity required the presence of Ca2+ at the cytosolic face but not the extracellular (endolymphatic) face; there was essentially no activity for cytosolic Ca2+ less than or equal to 10(-7) M Ca2+ and full activity for greater than or equal to 10(-5) M. Cell-attached recordings had a conductance of 28.6 +/- 2.2 pS (N = 6) and a reversal voltage of -2.2 +/- 5.2 mV (N = 3) which was interpreted to reflect the intracellular potential of marginal cells under the present conditions. The three other types of channel were a Cl- channel (approximately 50 pS; N = 2), a maxi-K+ channel (approximately 230 pS; N = 1), and another large channel, probably cation nonselective (approximately 170 pS; N = 1). The 27 pS nonselective cation channel may be involved in K+ secretion and Na+ absorption under stimulated conditions which produce an elevated intracellular Ca2+; however, consideration of the apparent channel density in relation to the total transepithelial K+ flux suggests that these channels are not sufficient to account for K+ secretion.
authors.affiliation: Biophysics Laboratory, Boys Town National Research Hospital, Omaha, Nebraska 68131.
authors.forename: S
authors.initials: S
authors.lastname: Takeuchi
authors.forename: D C
authors.initials: DC
authors.lastname: Marcus
authors.forename: P
authors.initials: P
authors.lastname: Wangemann
mesh_terms: D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D002413:Cations, Divalent / Q000378:metabolism; D002414:Cations, Monovalent / Q000378:metabolism; D018118:Chloride Channels; D002712:Chlorides / Q000378:metabolism; D004553:Electric Conductivity; D004594:Electrophysiology; D005849:Gerbillinae; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism*; D008565:Membrane Proteins / Q000187:drug effects / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism*; D013316:Stria Vascularis / Q000166:cytology / Q000378:metabolism*
chemical_list: D002413:Cations, Divalent; D002414:Cations, Monovalent; D018118:Chloride Channels; D002712:Chlorides; D007473:Ion Channels; D008565:Membrane Proteins; D015221:Potassium Channels; D011188:Potassium; D002118:Calcium