J Physiol Society Membership
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Physiol Vol 425 pp 347-367
Copyright © 1990 by The Physiological Society
This Article
Right arrow Full Text (PDF)
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Feldmeyer, D
Right arrow Articles by Zöllner, P
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Feldmeyer, D
Right arrow Articles by Zöllner, P

Fast gating kinetics of the slow Ca2+ current in cut skeletal muscle fibres of the frog.

D Feldmeyer, W Melzer, B Pohl and P Zöllner

Department of Cell Physiology, Ruhr-University Bochum, FRG.

1. Calcium currents and intramembrane charge movements were measured in cut twitch muscle fibres of the frog and the time course of activation of the current was studied using various conditioning pulse protocols. 2. When a conditioning activation was produced by a depolarizing pulse which ended before inactivation occurred, a subsequent depolarization led to a faster onset of activation, indicating that the system had not completely returned to the initial state during the interval between the two pulses. 3. The interval between conditioning and test pulse was varied at different subthreshold potentials to study the time course of restoring the steady-state conditions. Complete restoration required a waiting period of about 1 min at the holding potential of -80 mV due to a very slow process but partial recovery was reached within 100 ms. This initial recovery process was strongly voltage dependent and became considerably slower when the interval potential approached the threshold for current activation. 4. Stepping to a roughly 10 mV subthreshold potential without applying a conditioning activation caused no change in the time course of the current produced by a subsequent test depolarization. Depolarizing just to the current threshold caused a slowly progressing acceleration of test current activation. 5. The peak current-voltage relation in the fast gating regime caused by a conditioning activation coincided with the current-voltage relation measured under steady-state conditions, indicating not that a new channel population had become activated but that the same channels showed a different gating behaviour. 6. Intramembrane charge movements measured in 2 mM-Cd2+ and tested at potentials between -40 and +40 mV showed negligible changes when preceded by a strong depolarization. 7. We discuss several possible models which can explain the fact that the current is speeded up by a conditioning activation while the charge movements remain unchanged. It is possible that the fast voltage-dependent transition which becomes visible after conditioning pulses reflects a rapid conformational change of the Ca2+ channel molecule which also occurs during its normal gating mode but remains undetectable in terms of conductance. In view of the hypothesis that the Ca2+ channel molecule forms a voltage sensor for excitation-contraction coupling this fast transition could be coupled to the control of Ca2+ release from the sarcoplasmic reticulum.




This article has been cited by other articles:


Home page
Biophys. JHome page
C. J. Doering, J. Hamid, B. Simms, J. E. McRory, and G. W. Zamponi
Cav1.4 Encodes a Calcium Channel with Low Open Probability and Unitary Conductance
Biophys. J., November 1, 2005; 89(5): 3042 - 3048.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Cell Physiol.Home page
A. Shtifman, C. Paolini, J. R. Lopez, P. D. Allen, and F. Protasi
Ca2+ influx through {alpha}1S DHPR may play a role in regulating Ca2+ release from RyR1 in skeletal muscle
Am J Physiol Cell Physiol, January 1, 2004; 286(1): C73 - C78.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Cell Physiol.Home page
E. H. Lee, J. R. Lopez, J. Li, F. Protasi, I. N. Pessah, D. H. Kim, and P. D. Allen
Conformational coupling of DHPR and RyR1 in skeletal myotubes is influenced by long-range allosterism: evidence for a negative regulatory module
Am J Physiol Cell Physiol, January 1, 2004; 286(1): C179 - C189.
[Abstract] [Full Text] [PDF]


Home page
Biophys. JHome page
N. Kasielke, G. J. Obermair, G. Kugler, M. Grabner, and B. E. Flucher
Cardiac-type EC-Coupling in Dysgenic Myotubes Restored with Ca2+ Channel Subunit Isoforms {alpha}1C and {alpha}1D Does not Correlate with Current Density
Biophys. J., June 1, 2003; 84(6): 3816 - 3828.
[Abstract] [Full Text] [PDF]


Home page
J. Neurosci.Home page
J. A. Morrill, R. H. Brown Jr, and S. C. Cannon
Gating of the L-Type Ca Channel in Human Skeletal Myotubes: An Activation Defect Caused by the Hypokalemic Periodic Paralysis Mutation R528H
J. Neurosci., December 15, 1998; 18(24): 10320 - 10334.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
J. Zhou, L. Cribbs, J. Yi, R. Shirokov, E. Perez-Reyes, and E. Rios
Molecular Cloning and Functional Expression of a Skeletal Muscle Dihydropyridine Receptor from Rana catesbeiana
J. Biol. Chem., September 25, 1998; 273(39): 25503 - 25509.
[Abstract] [Full Text] [PDF]


Home page
J. Neurosci.Home page
B. D. Johnson, J. P. Brousal, B. Z. Peterson, P. A. Gallombardo, G. H. Hockerman, Y. Lai, T. Scheuer, and W. A. Catterall
Modulation of the Cloned Skeletal Muscle L-Type Ca2+ Channel by Anchored cAMP-Dependent Protein Kinase
J. Neurosci., February 15, 1997; 17(4): 1243 - 1255.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1990 The Physiological Society.