WWW.JNEUROSCI.ORG
-
The Journal of Neuroscience
QUICK SEARCH:   [advanced]


     
-


HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP
The Journal of Neuroscience, July 9, 2003, 23(14):6041-6049

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit an eLetter
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (48)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Koschak, A.
Right arrow Articles by Striessnig, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Koschak, A.
Right arrow Articles by Striessnig, J.

 Previous Article  |  Next Article 

Cav1.4{alpha}1 Subunits Can Form Slowly Inactivating Dihydropyridine-Sensitive L-Type Ca2+ Channels Lacking Ca2+-Dependent Inactivation

Alexandra Koschak,1 Daniel Reimer,1,2 Doris Walter,1 Jean-Charles Hoda,1 Thomas Heinzle,2 Manfred Grabner,2 and Jörg Striessnig1

1Institut für Pharmazie, Abteilung Pharmakologie und Toxikologie, A-6020 Innsbruck, Austria,2Institut für Biochemische Pharmakologie, A-6020 Innsbruck, Austria

The neuronal L-type calcium channels (LTCCs) Cav1.2{alpha}1 and Cav1.3{alpha}1 are functionally distinct. Cav1.3{alpha}1 activates at lower voltages and inactivates more slowly than Cav1.2{alpha}1, making it suitable to support sustained L-type Ca2+ inward currents (ICa,L) and serve in pacemaker functions. We compared the biophysical and pharmacological properties of human retinal Cav1.4{alpha}1 using the whole-cell patch-clamp technique after heterologous expression in tsA-201 cells with other L-type {alpha}1 subunits. Cav1.4{alpha}1-mediated inward Ba2+ currents (IBa) required the coexpression of {alpha}2{delta}1 and {beta}3 or {beta}2a subunits and were detected in a lower proportion of transfected cells than Cav1.3{alpha}1. IBa activated at more negative voltages (5% activation threshold; -39mV; 15 mM Ba2+) than Cav1.2{alpha}1 and slightly more positive than Cav1.3{alpha}1. Voltage-dependent inactivation of IBa was slower than for Cav1.2{alpha}1 and Cav1.3{alpha}1(~50% inactivation after 5 sec; {alpha}2{delta}1 + {beta}3 coexpression). Inactivation was not increased with Ca2+ as the charge carrier, indicating the absence of Ca2+-dependent inactivation. Cav1.4{alpha}1 exhibited voltage-dependent, G-protein-independent facilitation by strong depolarizing pulses. The dihydropyridine (DHP)-antagonist isradipine blocked Cav1.4{alpha}1 with ~15-fold lower sensitivity than Cav1.2{alpha}1 and in a voltage-dependent manner. Strong stimulation by the DHP BayK 8644 was found despite the substitution of an otherwise L-type channel-specific tyrosine residue in position 1414 (repeat IVS6) by a phenylalanine. Cav1.4{alpha}1 + {alpha}2{delta}1 + {beta} channel complexes can form LTCCs with intermediate DHP antagonist sensitivity lacking Ca2+-dependent inactivation. Their biophysical properties should enable them to contribute to sustained ICa,L at negative potentials, such as required for tonic neurotransmitter release in sensory cells and plateau potentials in spiking neurons.

Key words: calcium channels; calcium-dependent inactivation; retina; calcium channel blockers; dihydropyridines; congenital stationary night blindness

Received Jan. 21, 2003; revised Apr. 16, 2003; accepted Apr. 24, 2003.




This article has been cited by other articles:


Home page
 IOVSHome page
D. Specht, S.-B. Wu, P. Turner, P. Dearden, F. Koentgen, U. Wolfrum, M. Maw, J. H. Brandstatter, and S. tom Dieck
Effects of Presynaptic Mutations on a Postsynaptic Cacna1s Calcium Channel Colocalized with mGluR6 at Mouse Photoreceptor Ribbon Synapses
Invest. Ophthalmol. Vis. Sci., February 1, 2009; 50(2): 505 - 515.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Pharmacol.Home page
M. J. Sinnegger-Brauns, I. G. Huber, A. Koschak, C. Wild, G. J Obermair, U. Einzinger, J.-C. Hoda, S. B. Sartori, and J. Striessnig
Expression and 1,4-Dihydropyridine-Binding Properties of Brain L-Type Calcium Channel Isoforms
Mol. Pharmacol., February 1, 2009; 75(2): 407 - 414.
[Abstract] [Full Text] [PDF]

Home page
 PhysiologyHome page
H. Okawa and A. P. Sampath
Optimization of Single-Photon Response Transmission at the Rod-to-Rod Bipolar Synapse
Physiology, August 1, 2007; 22(4): 279 - 286.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
M. A. Diana, Y. Otsu, G. Maton, T. Collin, M. Chat, and S. Dieudonne
T-Type and L-Type Ca2+ Conductances Define and Encode the Bimodal Firing Pattern of Vestibulocerebellar Unipolar Brush Cells
J. Neurosci., April 4, 2007; 27(14): 3823 - 3838.
[Abstract] [Full Text] [PDF]

Home page
 Pharmacol. Rev.Home page
H. W. Tedford and G. W. Zamponi
Direct G Protein Modulation of Cav2 Calcium Channels
Pharmacol. Rev., December 1, 2006; 58(4): 837 - 862.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
C. Wahl-Schott, L. Baumann, H. Cuny, C. Eckert, K. Griessmeier, and M. Biel
Switching off calcium-dependent inactivation in L-type calcium channels by an autoinhibitory domain
PNAS, October 17, 2006; 103(42): 15657 - 15662.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
G. Baroudi, Y. Qu, O. Ramadan, M. Chahine, and M. Boutjdir
Protein kinase C activation inhibits Cav1.3 calcium channel at NH2-terminal serine 81 phosphorylation site.
Am J Physiol Heart Circ Physiol, October 1, 2006; 291(4): H1614 - H1622.
[Abstract] [Full Text] [PDF]

Home page
 J. Med. Genet.Home page
R Jalkanen, M Mantyjarvi, R Tobias, J Isosomppi, E-M Sankila, T Alitalo, and N T Bech-Hansen
X linked cone-rod dystrophy, CORDX3, is caused by a mutation in the CACNA1F gene
J. Med. Genet., August 1, 2006; 43(8): 699 - 704.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
H. Khosravani and G. W. Zamponi
Voltage-gated calcium channels and idiopathic generalized epilepsies.
Physiol Rev, July 1, 2006; 86(3): 941 - 966.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
A. Hohaus, S. Beyl, M. Kudrnac, S. Berjukow, E. N. Timin, R. Marksteiner, M. A. Maw, and S. Hering
Structural Determinants of L-type Channel Activation in Segment IIS6 Revealed by a Retinal Disorder
J. Biol. Chem., November 18, 2005; 280(46): 38471 - 38477.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
T. D. Helton, W. Xu, and D. Lipscombe
Neuronal L-Type Calcium Channels Open Quickly and Are Inhibited Slowly
J. Neurosci., November 2, 2005; 25(44): 10247 - 10251.
[Abstract] [Full Text] [PDF]

Home page
 IOVSHome page
T. Maeda, J. Lem, K. Palczewski, and F. Haeseleer
A Critical Role of CaBP4 in the Cone Synapse
Invest. Ophthalmol. Vis. Sci., November 1, 2005; 46(11): 4320 - 4327.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
A. Hemara-Wahanui, S. Berjukow, C. I. Hope, P. K. Dearden, S.-B. Wu, J. Wilson-Wheeler, D. M. Sharp, P. Lundon-Treweek, G. M. Clover, J.-C. Hoda, et al.
A CACNA1F mutation identified in an X-linked retinal disorder shifts the voltage dependence of Cav1.4 channel activation
PNAS, May 24, 2005; 102(21): 7553 - 7558.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
N. Hosoi, I. Arai, and M. Tachibana
Group III Metabotropic Glutamate Receptors and Exocytosed Protons Inhibit L-Type Calcium Currents in Cones But Not in Rods
J. Neurosci., April 20, 2005; 25(16): 4062 - 4072.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
J.-C. Hoda, F. Zaghetto, A. Koschak, and J. Striessnig
Congenital Stationary Night Blindness Type 2 Mutations S229P, G369D, L1068P, and W1440X Alter Channel Gating or Functional Expression of Cav1.4 L-type Ca2+ Channels
J. Neurosci., January 5, 2005; 25(1): 252 - 259.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurophysiol.Home page
D. Lipscombe, T. D. Helton, and W. Xu
L-Type Calcium Channels: The Low Down
J Neurophysiol, November 1, 2004; 92(5): 2633 - 2641.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
A. Agoston, L. Kunz, A. Krieger, and A. Mayerhofer
Two Types of Calcium Channels in Human Ovarian Endocrine Cells: Involvement in Steroidogenesis
J. Clin. Endocrinol. Metab., September 1, 2004; 89(9): 4503 - 4512.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
J. E. McRory, J. Hamid, C. J. Doering, E. Garcia, R. Parker, K. Hamming, L. Chen, M. Hildebrand, A. M. Beedle, L. Feldcamp, et al.
The CACNA1F Gene Encodes an L-Type Calcium Channel with Unique Biophysical Properties and Tissue Distribution
J. Neurosci., February 18, 2004; 24(7): 1707 - 1718.
[Abstract] [Full Text] [PDF]

Home page
 IOVSHome page
L. Baumann, A. Gerstner, X. Zong, M. Biel, and C. Wahl-Schott
Functional Characterization of the L-type Ca2+ Channel Cav1.4{alpha}1 from Mouse Retina
Invest. Ophthalmol. Vis. Sci., February 1, 2004; 45(2): 708 - 713.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
A. Brandt, J. Striessnig, and T. Moser
CaV1.3 Channels Are Essential for Development and Presynaptic Activity of Cochlear Inner Hair Cells
J. Neurosci., November 26, 2003; 23(34): 10832 - 10840.
[Abstract] [Full Text] [PDF]


-
-

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help
-
Copyright 2009 by Society for Neuroscience ONLINE ISSN: 1529-2401
-