Vestibular Dark Cells Contain an H + /Monocarboxylate − Cotransporter in Their Apical and Basolateral Membrane

1998 ◽  
Vol 163 (1) ◽  
pp. 37-46 ◽  
Author(s):  
M. Shimozono ◽  
J. Liu ◽  
M.A. Scofield ◽  
P. Wangemann
Keyword(s):  
Basolateral Membrane ◽  
Dark Cells ◽  
Vestibular Dark Cells

Vestibular dark cells contain the exchanger NHE-1 in the basolateral membrane

1996 ◽  
Vol 94 (1-2) ◽  
pp. 94-106 ◽  
Author(s):  
Philine Wangemann ◽  
Jianzhong Liu ◽  
Nobuyuki Shiga
Keyword(s):  
Basolateral Membrane ◽  
Dark Cells ◽  
Vestibular Dark Cells

Two types of chloride channel in the basolateral membrane of vestibular dark cells

1993 ◽  
Vol 69 (1-2) ◽  
pp. 124-132 ◽  
Author(s):  
Daniel C. Marcus ◽  
Shunji Takeuchi ◽  
Philine Wangemann
Keyword(s):  
Chloride Channel ◽  
Basolateral Membrane ◽  
Dark Cells ◽  
Vestibular Dark Cells

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.

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.

Otoconia on the Vestibular Dark Cells of the Ampullar Areas

1995 ◽  
Vol 115 (sup519) ◽  
pp. 140-142 ◽  
Author(s):  
Mamoru Fujii ◽  
Yasuo Harada ◽  
Katsuhiro Hirakawa ◽  
Masaya Takumida
Keyword(s):  
Dark Cells ◽  
Vestibular Dark Cells

Formation and Fate of the Otoconia

1973 ◽  
Vol 82 (1) ◽  
pp. 23-35 ◽  
Author(s):  
David J. Lim
Keyword(s):  
Calcium Carbonate ◽  
Organic Matrix ◽  
Laboratory Animals ◽  
Dark Cell ◽  
Gelatin Matrix ◽  
Dark Cells ◽  
The Matrix ◽  
Electron Microscopes ◽  
Vestibular Dark Cells ◽  
Clinical Conditions

Although mammalian otoconia are known to be composed of calcium carbonate in calcite form, their morphogenesis, maintenance, and fate are not well understood. More information on these problem areas would aid considerably in better understanding various clinical conditions, such as cupulolithiasis and otolith degeneration. This study was intended to clarify the fine morphology of the otolith in normal and adverse conditions in laboratory animals with the use of the scanning and transmission electron microscopes. It was confirmed by this study that the mammalian otoconium is composed of an organic matrix and minerals (calcium carbonate). When the minerals are removed by decalcification, or chelation, a well arranged organic matrix, and even a nucleus, can be found in the crystal. The matrix of the crystal is identical to the gelatin matrix of the otolithic membrane. This finding supports the possibility that a normal protein matrix is a prerequisite for normal otoconia formation, and that the exchange of calcium ions can occur without altering the crystal structure. The vestibular dark cells, which are thought to be endolymph-secreting cells, appear to be capable of removing calcium from the otoconia that are attached to the dark cell surfaces. Although this evidence is only circumstantial, its consistency is impressive. On the basis of the foregoing, it is tempting to speculate that the dark cells participate in the removal of the dislodged otoliths, but further study is required to ascertain this point.

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