The whole-cell patch-clamp technique was used to study the properties of inward ionic currents found in primary cultures of rat and mouse skeletal myotubes and in freshly dissociated fibers of the flexor digitorum brevis muscle of rats. In each of these cell types, test depolarizations from the holding potential (-80 or -90 mV) elicited three distinct inward currents: a sodium current (INa) and two calcium currents. INa was the dominant inward current: under physiological conditions, the maximum inward INa was estimated to be at least 30-fold larger than either of the calcium currents. The two calcium currents have been termed Ifast and Islow, corresponding to their relative rates of activation. Ifast was activated by test depolarizations to around -40 mV and above, peaked in 10-20 ms, and decayed to baseline in 50-100 ms. Islow was activated by depolarizations to approximately 0 mV and above, peaked in 50-150 ms, and decayed little during a 200-ms test pulse. Ifast was inactivated by brief, moderate depolarizations; for a 1-s change in holding potential, half-inactivation occurred at -55 to -45 mV and complete inactivation occurred at -40 to -30 mV. Similar changes in holding potential had no effect on Islow. Islow was, however, inactivated by brief, strong depolarizations (e.g., 0 mV for 2 s) or maintained, moderate depolarizations (e.g., -40 mV for 60 s). Substitution of barium for calcium had little effect on the magnitude or time course of either Ifast or Islow. The same substitution shifted the activation curve for Islow approximately 10 mV in the hyperpolarizing direction without affecting the activation of Ifast. At low concentrations (50 microM), cadmium preferentially blocked Islow compared with Ifast, while at high concentrations (1 mM), it blocked both Ifast and Islow completely. The dihydropyridine calcium channel antagonist (+)-PN 200-110 (1 microM) caused a nearly complete block of Islow without affecting Ifast. At a holding potential of -80 mV, the half-maximal blocking concentration (K0.5) for the block of Islow by (+)-PN 200-110 was 182 nM. At depolarized holding potentials that inactivated Islow by 35-65%, K0.5 decreased to 5.5 nM.
CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				J. Ohrtman, B. Ritter, A. Polster, K. G. Beam, and S. Papadopoulos Sequence Differences in the IQ Motifs of CaV1.1 and CaV1.2 Strongly Impact Calmodulin Binding and Calcium-dependent Inactivation J. Biol. Chem., October 24, 2008; 283(43): 29301 - 29311. [Abstract] [Full Text] [PDF]

				K. Hacker and K. F. Medler Mitochondrial Calcium Buffering Contributes to the Maintenance of Basal Calcium Levels in Mouse Taste Cells J Neurophysiol, October 1, 2008; 100(4): 2177 - 2191. [Abstract] [Full Text] [PDF]

				K. Hacker, A. Laskowski, L. Feng, D. Restrepo, and K. Medler Evidence for Two Populations of Bitter Responsive Taste Cells in Mice J Neurophysiol, March 1, 2008; 99(3): 1503 - 1514. [Abstract] [Full Text] [PDF]

				E. Bandi, M. Jevsek, T. Mars, M. Jurdana, E. Formaggio, M. Sciancalepore, G. Fumagalli, Z. Grubic, F. Ruzzier, and P. Lorenzon Neural agrin controls maturation of the excitation-contraction coupling mechanism in human myotubes developing in vitro Am J Physiol Cell Physiol, January 1, 2008; 294(1): C66 - C73. [Abstract] [Full Text] [PDF]

				J. D. Lueck, C. Lungu, A. Mankodi, R. J. Osborne, S. L. Welle, R. T. Dirksen, and C. A. Thornton Chloride channelopathy in myotonic dystrophy resulting from loss of posttranscriptional regulation for CLCN1 Am J Physiol Cell Physiol, April 1, 2007; 292(4): C1291 - C1297. [Abstract] [Full Text] [PDF]

				J. D. Lueck, A. Mankodi, M. S. Swanson, C. A. Thornton, and R. T. Dirksen Muscle Chloride Channel Dysfunction in Two Mouse Models of Myotonic Dystrophy J. Gen. Physiol., January 1, 2007; 129(1): 79 - 94. [Abstract] [Full Text] [PDF]

				I. M.-P. y Valenzuela, R. I. Hume, E. Krejci, and M. Akaaboune In Vivo Regulation of Acetylcholinesterase Insertion at the Neuromuscular Junction J. Biol. Chem., September 9, 2005; 280(36): 31801 - 31808. [Abstract] [Full Text] [PDF]

				F. P. Elsen and J.-M. Ramirez Postnatal Development Differentially Affects Voltage-Activated Calcium Currents in Respiratory Rhythmic Versus Nonrhythmic Neurons of the Pre-Botzinger Complex J Neurophysiol, August 1, 2005; 94(2): 1423 - 1431. [Abstract] [Full Text] [PDF]

				J. Capote, P. Bolanos, R. P. Schuhmeier, W. Melzer, and C. Caputo Calcium transients in developing mouse skeletal muscle fibres J. Physiol., April 15, 2005; 564(2): 451 - 464. [Abstract] [Full Text] [PDF]

				G. Cherednichenko, A. M. Hurne, J. D. Fessenden, E. H. Lee, P. D. Allen, K. G. Beam, and I. N. Pessah Conformational activation of Ca2+ entry by depolarization of skeletal myotubes PNAS, November 2, 2004; 101(44): 15793 - 15798. [Abstract] [Full Text] [PDF]

				L. Mejia-Luna and G. Avila Ca2+ channel regulation by transforming growth factor-{beta}1 and bone morphogenetic protein-2 in developing mice myotubes J. Physiol., August 15, 2004; 559(1): 41 - 54. [Abstract] [Full Text] [PDF]

				H. C. Ott, S. Berjukow, R. Marksteiner, E. Margreiter, G. Bock, G. Laufer, and S. Hering On the fate of skeletal myoblasts in a cardiac environment: down-regulation of voltage-gated ion channels J. Physiol., August 1, 2004; 558(3): 793 - 805. [Abstract] [Full Text] [PDF]

				V. Leuranguer, R. T. Dirksen, and K. G. Beam Potentiated L-type Ca2+ Channels Rectify J. Gen. Physiol., May 27, 2003; 121(6): 541 - 550. [Abstract] [Full Text] [PDF]

				Z. Zheng, Z.-M. Wang, and O. Delbono Insulin-like Growth Factor-1 Increases Skeletal Muscle Dihydropyridine Receptor alpha 1S Transcriptional Activity by Acting on the cAMP-response Element-binding Protein Element of the Promoter Region J. Biol. Chem., December 20, 2002; 277(52): 50535 - 50542. [Abstract] [Full Text] [PDF]

				K. Ito, S. Komazaki, K. Sasamoto, M. Yoshida, M. Nishi, K. Kitamura, and H. Takeshima Deficiency of triad junction and contraction in mutant skeletal muscle lacking junctophilin type 1 J. Cell Biol., September 3, 2001; 154(5): 1059 - 1068. [Abstract] [Full Text] [PDF]

				D. Freise, B. Held, U. Wissenbach, A. Pfeifer, C. Trost, N. Himmerkus, U. Schweig, M. Freichel, M. Biel, F. Hofmann, et al. Absence of the gamma Subunit of the Skeletal Muscle Dihydropyridine Receptor Increases L-type Ca2+ Currents and Alters Channel Inactivation Properties J. Biol. Chem., May 5, 2000; 275(19): 14476 - 14481. [Abstract] [Full Text] [PDF]

				C. Menard, S. Pupier, D. Mornet, M. Kitzmann, J. Nargeot, and P. Lory Modulation of L-type Calcium Channel Expression during Retinoic Acid-induced Differentiation of H9C2 Cardiac Cells J. Biol. Chem., October 8, 1999; 274(41): 29063 - 29070. [Abstract] [Full Text] [PDF]

				F. Lehmann-Horn and K. Jurkat-Rott Voltage-Gated Ion Channels and Hereditary Disease Physiol Rev, October 1, 1999; 79(4): 1317 - 1372. [Abstract] [Full Text] [PDF]

				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]

				R. D. Zuhlke and H. Reuter Ca2+-sensitive inactivation of L-type Ca2+ channels depends on multiple cytoplasmic amino acid sequences of the alpha 1C subunit PNAS, March 17, 1998; 95(6): 3287 - 3294. [Abstract] [Full Text] [PDF]

				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]

				H. Widmer, H. Amerdeil, P. Fontanaud, and M. G. Desarmenien Postnatal Maturation of Rat Hypothalamoneurohypophysial Neurons: Evidence for a Developmental Decrease in Calcium Entry During Action Potentials J Neurophysiol, January 1, 1997; 77(1): 260 - 271. [Abstract] [Full Text] [PDF]

				W. H. Frishman Mibefradil: A New Selective T-Channel Calcium Antagonist for Hypertension and Angina Pectoris Journal of Cardiovascular Pharmacology and Therapeutics, January 1, 1997; 2(4): 321 - 330. [Abstract] [PDF]

				K. D. Garcia and K. G. Beam Reduction of Calcium Currents by Lambert-Eaton Syndrome Sera: Motoneurons Are Preferentially Affected, and L-Type Currents Are Spared J. Neurosci., August 15, 1996; 16(16): 4903 - 4913. [Abstract] [Full Text] [PDF]

				E. Bourinet, G. W. Zamponi, A. Stea, T. W. Soong, B. A. Lewis, L. P. Jones, D. T. Yue, and T. P. Snutch The alpha 1E Calcium Channel Exhibits Permeation Properties Similar to Low-Voltage-Activated Calcium Channels J. Neurosci., August 15, 1996; 16(16): 4983 - 4993. [Abstract] [Full Text] [PDF]

				C Cognard, B Constantin, M Rivet-Bastide, N Imbert, C Besse, and G Raymond Appearance and evolution of calcium currents and contraction during the early post-fusional stages of rat skeletal muscle cells developing in primary culture Development, January 3, 1993; 117(3): 1153 - 1161. [Abstract] [PDF]

				G. Avila, K. M. S. O'Connell, L. A. Groom, and R. T. Dirksen Ca2+ Release through Ryanodine Receptors Regulates Skeletal Muscle L-type Ca2+ Channel Expression J. Biol. Chem., May 18, 2001; 276(21): 17732 - 17738. [Abstract] [Full Text] [PDF]

				B. Held, D. Freise, M. Freichel, M. Hoth, and V. Flockerzi Skeletal muscle L-type Ca2+ current modulation in gamma1-deficient and wildtype murine myotubes by the gamma1 subunit and cAMP J. Physiol., March 1, 2002; 539(2): 459 - 468. [Abstract] [Full Text] [PDF]

				C. Berthier, A. Monteil, P. Lory, and C. Strube alpha1H mRNA in single skeletal muscle fibres accounts for T-type calcium current transient expression during fetal development in mice J. Physiol., March 15, 2002; 539(3): 681 - 691. [Abstract] [Full Text] [PDF]

				Z. Zheng, Z.-M. Wang, and O. Delbono Charge movement and transcription regulation of L-type calcium channel alpha1S in skeletal muscle cells J. Physiol., April 15, 2002; 540(2): 397 - 409. [Abstract] [Full Text] [PDF]

Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents