scholarly journals Biophysical and Pharmacological Characterization of Voltage‐Gated Calcium Currents in Turtle Auditory Hair Cells

2003 ◽  
Vol 549 (3) ◽  
pp. 697-717 ◽  
Author(s):  
M. E. Schnee ◽  
A. J. Ricci
Keyword(s):  
Hair Cells ◽  
Calcium Currents ◽  
Pharmacological Characterization ◽  
Auditory Hair Cells ◽  
Voltage Gated

Calcium- and Calmodulin-Dependent Inactivation of Calcium Channels in Inner Hair Cells of the Rat Cochlea

2008 ◽  
Vol 99 (5) ◽  
pp. 2183-2193 ◽  
Author(s):  
Lisa Grant ◽  
Paul Fuchs
Keyword(s):  
Calcium Channels ◽  
Hair Cells ◽  
Calcium Currents ◽  
Resting Potential ◽  
Resting Membrane Potential ◽  
Inner Hair Cells ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Dependent Inactivation ◽  
Calcium Buffering

Modulation of voltage-gated calcium channels was studied in inner hair cells (IHCs) in an ex vivo preparation of the apical turn of the rat organ of Corti. Whole cell voltage clamp in the presence of potassium channel blockers showed inward calcium currents with millisecond activation and deactivation kinetics. When temperature was raised from 22 to 37°C, the calcium currents of immature IHCs [<12 days postnatal (P12)] increased threefold in amplitude, and developed more pronounced inactivation. This was determined to be calcium-dependent inactivation (CDI) on the basis of its reliance on external calcium (substitution with barium), sensitivity to internal calcium-buffering, and voltage dependence (reflecting the calcium driving force). After the onset of hearing at P12, IHC calcium current amplitude and the extent of inactivation were greatly reduced. Although smaller than in prehearing IHCs, CDI remained significant in the mature IHC near the resting membrane potential. CDI in mature IHCs was enhanced by application of the endoplasmic calcium pump blocker, benzo-hydroquinone. Conversely, CDI in immature IHCs was reduced by calmodulin inhibitors. Thus voltage-gated calcium channels in mammalian IHCs are subject to a calmodulin-mediated process of CDI. The extent of CDI depends on the balance of calcium buffering mechanisms and may be regulated by calmodulin-specific processes. CDI provides a means for the rate of spontaneous transmitter release to be adjusted to variations in hair cell resting potential and steady state calcium influx.

Characterization of biological effect of 1763 MHz radiofrequency exposure on auditory hair cells

2008 ◽  
Vol 84 (11) ◽  
pp. 909-915 ◽  
Author(s):  
Tai-Qin Huang ◽  
Min Su Lee ◽  
Eun-Ha Oh ◽  
Federico Kalinec ◽  
Byoung-Tak Zhang ◽  
...  
Keyword(s):  
Hair Cells ◽  
Biological Effect ◽  
Auditory Hair Cells

Inhibition of voltage-gated calcium currents in type II vestibular hair cells by cinnarizine

2004 ◽  
Vol 369 (6) ◽  
pp. 570-575 ◽  
Author(s):  
Sonja F. Arab ◽  
Philip D�wel ◽  
Eberhard J�ngling ◽  
Martin Westhofen ◽  
Andreas L�ckhoff
Keyword(s):  
Hair Cells ◽  
Calcium Currents ◽  
Type Ii ◽  
Voltage Gated ◽  
Vestibular Hair Cells

Pharmacological characterization of two calcium currents in GH3 cells

1988 ◽  
Vol 254 (3) ◽  
pp. E328-E336 ◽  
Author(s):  
S. M. Simasko ◽  
G. A. Weiland ◽  
R. E. Oswald
Keyword(s):  
Channel Blocker ◽  
Pituitary Cell ◽  
Calcium Currents ◽  
Gh3 Cells ◽  
Pharmacological Properties ◽  
Pharmacological Characterization ◽  
Whole Cell Patch Clamp ◽  
Rat Pituitary ◽  
Dihydropyridine Calcium Channel Blocker

Whole cell patch-clamp techniques were used to investigate the pharmacological properties of calcium currents in the clonal rat pituitary cell line GH3. Current traces induced by a 100-ms pulse to 0 mV from a holding potential of -80 mV consisted of a component that rapidly inactivated during the pulse and a component that slowly inactivated during the pulse. When the holding potential was reduced to -32 mV, the rapidly inactivating component of the trace disappeared. The dihydropyridine calcium channel blocker nitrendipine affected only the slowly inactivating component of the trace. At a holding potential of -80 mV, nitrendipine blocked the slowly inactivating current with an IC50 of 1 microM. The IC50 for nitrendipine was found to be dependent on the holding potential, decreasing to 10 nM when the holding potential was -32 mV. The dihydropyridine agonist Bay-K 8644, like nitrendipine, affected only the slowly inactivating component. The inorganic blocker Cd2+ blocked both components but the slowly inactivating current was three- to fourfold more sensitive. These results are best explained by the existence of two types of calcium channels in these cells, one sensitive to dihydropyridines and one insensitive to dihydropyridines. These channels appear analogous to the T-type channel (inactivating current) and L-type channel (slowly inactivating current) described in other preparations.

Sign in / Sign up

Export Citation Format

Share Document