Calcium-dependent inactivation of neuronal calcium channels

2002 ◽  
Vol 3 (11) ◽  
pp. 873-883 ◽  
Author(s):  
Thomas Budde ◽  
Sven Meuth ◽  
Hans-Christian Pape
Keyword(s):  
Calcium Channels ◽  
Calcium Dependent ◽  
Dependent Inactivation ◽  
Neuronal Calcium Channels

scholarly journals Calcium-dependent inactivation of the dihydropyridine-sensitive calcium channels in GH3 cells.

1988 ◽  
Vol 92 (4) ◽  
pp. 531-548 ◽  
Author(s):  
D Kalman ◽  
P H O'Lague ◽  
C Erxleben ◽  
D L Armstrong
Keyword(s):  
Calcium Channels ◽  
Calcium Current ◽  
State Level ◽  
Gh3 Cells ◽  
Free Calcium ◽  
Pipette Solution ◽  
Calcium Dependent ◽  
Dependent Inactivation ◽  
Exogenous Calcium ◽  
Free Membrane

The inactivation of calcium channels in mammalian pituitary tumor cells (GH3) was studied with patch electrodes under voltage clamp in cell-free membrane patches and in dialyzed cells. The calcium current elicited by depolarization from a holding potential of -40 mV passed predominantly through one class of channels previously shown to be modulated by dihydropyridines and cAMP-dependent phosphorylation (Armstrong and Eckert, 1987). When exogenous calcium buffers were omitted from the pipette solution, the macroscopic calcium current through those channels inactivated with a half time of approximately 10 ms to a steady state level 40-75% smaller than the peak. Inactivation was also measured as the reduction in peak current during a test pulse that closely followed a prepulse. Inactivation was largely reduced or eliminated by (a) buffering free calcium in the pipette solution to less than 10(-8) M; (b) replacing extracellular calcium with barium; (c) increasing the prepulse voltage from +10 to +60 mV; or (d) increasing the intracellular concentration of cAMP, either 'directly' with dibutyryl-cAMP or indirectly by activating adenylate cyclase with forskolin or vasoactive intestinal peptide. Thus, inactivation of the dihydropyridine-sensitive calcium channels in GH3 cells only occurs when membrane depolarization leads to calcium ion entry and intracellular accumulation.

scholarly journals Localized Calcineurin in Calcium- Dependent Inactivation of L-type Calcium Channels

2010 ◽  
Vol 98 (3) ◽  
pp. 692a
Author(s):  
William A. Sather ◽  
Seth F. Oliveria ◽  
Mark L. Dell'Acqua
Keyword(s):  
Calcium Channels ◽  
Calcium Dependent ◽  
Dependent Inactivation

scholarly journals Switching off calcium-dependent inactivation in L-type calcium channels by an autoinhibitory domain

2006 ◽  
Vol 103 (42) ◽  
pp. 15657-15662 ◽  
Author(s):  
C. Wahl-Schott ◽  
L. Baumann ◽  
H. Cuny ◽  
C. Eckert ◽  
K. Griessmeier ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Autoinhibitory Domain ◽  
Calcium Dependent ◽  
Dependent Inactivation

scholarly journals Calcium-dependent inactivation of calcium channels in cochlear hair cells of the chicken

2007 ◽  
Vol 583 (3) ◽  
pp. 909-922 ◽  
Author(s):  
Seunghwan Lee ◽  
Olga Briklin ◽  
Hakim Hiel ◽  
Paul Fuchs
Keyword(s):  
Calcium Channels ◽  
Hair Cells ◽  
Cochlear Hair Cells ◽  
Calcium Dependent ◽  
Dependent Inactivation

scholarly journals Ser1928 is Required for Regulation of Calcium-Dependent Inactivation of CaV1.2 L-Type Calcium Channels by AKAP79-Anchored PKA and Calcineurin

2012 ◽  
Vol 102 (3) ◽  
pp. 128a
Author(s):  
Dong-ho Youn ◽  
Seth F. Oliveria ◽  
Mark L. Dell'Acqua ◽  
William A. Sather
Keyword(s):  
Calcium Channels ◽  
Calcium Dependent ◽  
Dependent Inactivation

scholarly journals Calcium-dependent inactivation of calcium channels in the medial striatum increases at eye opening

2015 ◽  
Vol 113 (7) ◽  
pp. 2979-2986 ◽  
Author(s):  
R. C. Evans ◽  
G. A. Herin ◽  
S. L. Hawes ◽  
K. T. Blackwell
Keyword(s):  
Calcium Channels ◽  
Developmental Stages ◽  
Calcium Influx ◽  
Age Groups ◽  
Calcium Dynamics ◽  
Striatal Neuron ◽  
Striatal Neurons ◽  
Calcium Dependent ◽  
Dependent Inactivation ◽  
Eye Opening

Influx of calcium through voltage-gated calcium channels (VGCCs) is essential for striatal function and plasticity. VGCCs expressed in striatal neurons have varying kinetics, voltage dependences, and densities resulting in heterogeneous subcellular calcium dynamics. One factor that determines the calcium dynamics in striatal medium spiny neurons is inactivation of VGCCs. Aside from voltage-dependent inactivation, VGCCs undergo calcium-dependent inactivation (CDI): inactivating in response to an influx of calcium. CDI is a negative feedback control mechanism; however, its contribution to striatal neuron function is unknown. Furthermore, although the density of VGCC expression changes with development, it is unclear whether CDI changes with development. Because calcium influx through L-type calcium channels is required for striatal synaptic depression, a change in CDI could contribute to age-dependent changes in striatal synaptic plasticity. Here we use whole cell voltage clamp to characterize CDI over developmental stages and across striatal regions. We find that CDI increases at the age of eye opening in the medial striatum but not the lateral striatum. The developmental increase in CDI mostly involves L-type channels, although calcium influx through non-L-type channels contributes to the CDI in both age groups. Agents that enhance protein kinase A (PKA) phosphorylation of calcium channels reduce the magnitude of CDI after eye opening, suggesting that the developmental increase in CDI may be related to a reduction in the phosphorylation state of the L-type calcium channel. These results are the first to show that modifications in striatal neuron properties correlate with changes to sensory input.

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