title: Basolateral K+ conductance establishes driving force for cation absorption by outer sulcus epithelial cells.
abstract: Outer sulcus epithelial cells were recently found to actively reabsorb cations from the cochlear luminal fluid, endolymph, via nonselective cation channels in the apical membrane. Here we determined the transport properties of the basolateral membrane with the whole-cell patch clamp technique; the apical membrane contributed insignificantly to the recordings. Outer sulcus epithelial cells exhibited both outward and inward currents and had a resting membrane potential of -90.4 +/- 0.7 mV (n = 78), close to the Nernst potential for K+ (-95 mV). The reversal potential depolarized by 54 mV for a tenfold increase in extracellular K+ concentration with a K+/Na+ permeability ratio of 36. The most frequently observed K+ current was voltage independent over a broad range of membrane potentials. The current was reduced by extracellular barium (10-5 to 10-3 m), amiloride (0.5 mm), quinine (1 mm), lidocaine (5 mm) and ouabain (1 mm). On the other hand, TEA (20 mm), charybdotoxin (100 nm), apamin (100 nm), glibenclamide (10 microm), 4-aminopyridine (1 mm) and gadolinium (1 mm) had no significant effect. These data suggest that the large K+ conductance, in concert with the Na+,K+-ATPase, of the basolateral membrane of outer sulcus cells provides the driving force for cation entry across the apical membrane, thereby energizing vectorial cation absorption by this epithelium and contributing to the homeostasis of endolymph.
authors.affiliation: Cellular Biophysics Laboratory, Anatomy & Physiology Dept., Kansas State University, Manhattan, KS 66506, USA.
authors.forename: T
authors.initials: T
authors.lastname: Chiba
authors.forename: D C
authors.initials: DC
authors.lastname: Marcus
mesh_terms: D000042:Absorption / Q000502:physiology; D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D001464:Barium / Q000494:pharmacology; D002414:Cations, Monovalent / Q000378:metabolism; D004553:Electric Conductivity; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004847:Epithelial Cells / Q000187:drug effects / Q000502:physiology*; D005849:Gerbillinae; D008012:Lidocaine / Q000494:pharmacology; D008564:Membrane Potentials / Q000502:physiology; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000378:metabolism*; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000502:physiology*; D011803:Quinine / Q000494:pharmacology; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D002414:Cations, Monovalent; D004791:Enzyme Inhibitors; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D001464:Barium; D000584:Amiloride; D008012:Lidocaine; D011803:Quinine; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium