β 1 -Adrenergic Receptors but not β 2 -Adrenergic or Vasopressin Receptors Regulate K + Secretion in Vestibular Dark Cells of the Inner Ear

1999 ◽  
Vol 170 (1) ◽  
pp. 67-77 ◽  
Author(s):  
P. Wangemann ◽  
J. Liu ◽  
M. Shimozono ◽  
M.A. Scofield
Keyword(s):  
Inner Ear ◽  
Adrenergic Receptors ◽  
Dark Cells ◽  
Vasopressin Receptors ◽  
K Secretion ◽  
Vestibular Dark Cells

Ca(2+)-activated nonselective cation channel in apical membrane of vestibular dark cells

1992 ◽  
Vol 262 (6) ◽  
pp. C1423-C1429 ◽  
Author(s):  
D. C. Marcus ◽  
S. Takeuchi ◽  
P. Wangemann
Keyword(s):  
Single Channel ◽  
Apical Membrane ◽  
Cation Channel ◽  
Nonselective Cation Channel ◽  
Channel Activity ◽  
Dark Cells ◽  
Linear Current ◽  
Current Voltage ◽  
K Secretion ◽  
Vestibular Dark Cells

Patch-clamp recordings were made on cell-attached and excised apical membrane from dark cells of the semicircular canal of the gerbil. These cells are thought to secrete K+ and absorb Na+ from the luminal fluid (endolymph). Single-channel events were identified as being equally conductive (27.6 +/- 0.4 pS; n = 48) for K+, Na+, Rb+, Li+, and Cs+ and 1.4 times more permeable to NH4+ but not permeable to Cl-, Ca2+, Ba2+, nor to N-methyl-D-glucamine. The channels displayed linear current-voltage relations that passed nearly through the origin (intercept: -2.6 +/- 0.5 mV; n = 48) 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; there was no activity at less than or equal to 10(-7) M Ca2+ and full activity at greater than or equal to 10(-5) M Ca2+. Cell-attached recordings had a mean reversal voltage of -36.4 +/- 7.9 mV (n = 7), which was interpreted to reflect the intracellular potential of dark cells under the present conditions. We have identified a nonselective cation channel in the apical membrane of vestibular dark cells that might participate in K+ secretion or Na+ absorption under stimulated conditions, but the density appears to be insufficient to fully account for the transepithelial K+ flux.

cAMP Increases Apical I sK Channel Current and K + Secretion in Vestibular Dark Cells

1997 ◽  
Vol 156 (1) ◽  
pp. 25-35 ◽  
Author(s):  
H. Sunose ◽  
J. Liu ◽  
Z. Shen ◽  
D.C. Marcus
Keyword(s):  
Dark Cells ◽  
Channel Current ◽  
Sk Channel ◽  
K Secretion ◽  
Vestibular Dark Cells

K+ Secretion in Strial Marginal Cells is Stimulated via β1-Adrenergic Receptors but not via β2-Adrenergic or Vasopressin Receptors

2000 ◽  
Vol 175 (3) ◽  
pp. 191-202 ◽  
Author(s):  
P. Wangemann ◽  
J. Liu ◽  
M. Shimozono ◽  
S. Schimanski ◽  
M.A. Scofield
Keyword(s):  
Adrenergic Receptors ◽  
Vasopressin Receptors ◽  
K Secretion ◽  
Marginal Cells

Stria vascularis and vestibular dark cells: characterisation of main structures responsible for inner-ear homeostasis, and their pathophysiological relations

2008 ◽  
Vol 123 (2) ◽  
pp. 151-162 ◽  
Author(s):  
R R Ciuman
Keyword(s):  
Inner Ear ◽  
Volume Concentration ◽  
Current Knowledge ◽  
Stria Vascularis ◽  
Dark Cells ◽  
Adequate Response ◽  
Complex Process ◽  
And Function ◽  
Vestibular Dark Cells ◽  
Distinct Morphology

AbstractThe regulation of inner-ear fluid homeostasis, with its parameters volume, concentration, osmolarity and pressure, is the basis for adequate response to stimulation. Many structures are involved in the complex process of inner-ear homeostasis. The stria vascularis and vestibular dark cells are the two main structures responsible for endolymph secretion, and possess many similarities. The characteristics of these structures are the basis for regulation of inner-ear homeostasis, while impaired function is related to various diseases. Their distinct morphology and function are described, and related to current knowledge of associated inner-ear diseases. Further research on the distinct function and regulation of these structures is necessary in order to develop future clinical interventions.

Evidence for the involvement of a K+ channel in isosmotic cell shrinking in vestibular dark cells

1992 ◽  
Vol 263 (3) ◽  
pp. C616-C622 ◽  
Author(s):  
P. Wangemann ◽  
N. Shiga ◽  
C. Welch ◽  
D. C. Marcus
Keyword(s):  
Initial Rate ◽  
Basolateral Membrane ◽  
Regulatory Volume Decrease ◽  
Cell Swelling ◽  
K Channel ◽  
Control Solution ◽  
Dark Cells ◽  
Physiological Relevance ◽  
K Secretion ◽  
Vestibular Dark Cells

Cell volume changes were measured in dark cells. Isosmotic addition of 21.4 mM K+, Rb+, Cs+, or NH4+ to a control solution containing 3.6 mM K+ caused piretanide-sensitive cell swelling (initial rate for K+, 0.100 +/- 0.005 microns/s; n = 119), suggesting dependence on the Na(+)-Cl(-)-K+ cotransporter. Subsequent isosmotic removal of 21.4 mM K+ caused piretanide-insensitive cell shrinking (initial rate, -0.104 +/- 0.005 microns/s; n = 119), which was inhibited by barium, lidocaine, quinidine, quinine, verapamil, and 4-aminopyridine but not tetraethylammonium (TEA) or glibenclamide, suggesting the involvement of K+ channel(s). Barium, lidocaine, quinine, quinidine, and 4-aminopyridine caused cell swelling in control solution (initial rate for barium, 0.011 +/- 0.004 microns/s; n = 6), suggesting that the K+ channel is also involved in efflux under control conditions. Cell shrinking was slowed by 21.4 mM extracellular K+, Rb+, or Cs+ but unaffected by Na+, Li+, TEA+, or NH4+ (all in the presence of piretanide and compared with N-methyl-D-glucamine), supporting the notion that the efflux mechanism is permeable to and/or inhibited by K+, Rb+, and Cs+. Cell shrinking was slowed by the presumed replacement of intracellular K+ by Cs+ but not by Rb+. Circumstantial evidence suggests that this putative K+ channel is present in the basolateral membrane. The physiological relevance of such a K+ channel might encompass regulatory volume decrease during K+ secretion.

K+-induced stimulation of K+ secretion involves activation of the IsK channel in vestibular dark cells

1996 ◽  
Vol 100 (1-2) ◽  
pp. 201-210 ◽  
Author(s):  
Philine Wangemann ◽  
Zhijun Shen ◽  
Jianzhong Liu
Keyword(s):  
Dark Cells ◽  
K Secretion ◽  
Vestibular Dark Cells ◽  
Stimulation Of

Computational model of vectorial potassium transport by cochlear marginal cells and vestibular dark cells

2007 ◽  
Vol 292 (1) ◽  
pp. C591-C602 ◽  
Author(s):  
Imran H. Quraishi ◽  
Robert M. Raphael
Keyword(s):  
Ion Transport ◽  
Inner Ear ◽  
Short Circuit ◽  
Ion Homeostasis ◽  
Bartter Syndrome ◽  
Dark Cell ◽  
Dark Cells ◽  
Type Iv ◽  
Marginal Cells ◽  
Vestibular Dark Cells

Cochlear marginal cells and vestibular dark cells transport potassium into the inner ear endolymph, a potassium-rich fluid, the homeostasis of which is essential for hearing and balance. We have formulated an integrated mathematical model of ion transport across these epithelia that incorporates the biophysical properties of the major ion transporters and channels located in the apical and basolateral membranes of the constituent cells. The model is constructed for both open- and short-circuit situations to test the extremes of functional capacity of the epithelium and predicts the steady-state voltages, ion concentrations, and transepithelial currents as a function of various transporter and channel densities. We validate the model by establishing that the cells are capable of vectorial ion transport consistent with several experimental measurements. The model indicates that cochlear marginal cells do not make a significant direct contribution to the endocochlear potential and illustrates how changes to the activity of specific transport proteins lead to reduced K+ flux across the marginal and dark cell layers. In particular, we investigate the mechanisms of loop diuretic ototoxicity and diseases with hearing loss in which K+ and Cl− transport are compromised, such as Jervell and Lange-Nielsen syndrome and Bartter syndrome, type IV, respectively. Such simulations demonstrate the utility of compartmental modeling in investigating the role of ion homeostasis in inner ear physiology and pathology.

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