|
||
The Journal of General Physiology, Vol 96, 689-706, Copyright © 1990 by The Rockefeller University Press
ARTICLES |
DS Krafte, AL Goldin, VJ Auld, RJ Dunn, N Davidson and HA Lester
Division of Biology, California Institute of Technology, Pasadena 91125.
This study investigates the inactivation properties of Na channels expressed in Xenopus oocytes from two rat IIA Na channel cDNA clones differing by a single amino acid residue. Although the two cDNAs encode Na channels with substantially different activation properties (Auld, V. J., A. L. Goldin, D. S. Krafte, J. Marshall, J. M. Dunn, W. A. Catterall, H. A. Lester, N. Davidson, and R. J. Dunn. 1988. Neuron. 1:449-461), their inactivation properties resemble each other strongly but differ markedly from channels induced by poly(A+) rat brain RNA. Rat IIA currents inactivate more slowly, recover from inactivation more slowly, and display a steady-state voltage dependence that is shifted to more positive potentials. The macroscopic inactivation process for poly(A+) Na channels is defined by a single exponential time course; that for rat IIA channels displays two exponential components. At the single-channel level these differences in inactivation occur because rat IIA channels reopen several times during a depolarizing pulse; poly(A+) channels do not. Repetitive stimulation (greater than 1 Hz) produces a marked decrement in the rat IIA peak current and changes the waveform of the currents. When low molecular weight RNA is coinjected with rat IIA RNA, these inactivation properties are restored to those that characterize poly(A+) channels. Slow inactivation is similar for rat IIA and poly(A+) channels, however. The data suggest that activation and inactivation involve at least partially distinct regions of the channel protein.
This article has been cited by other articles:
![]() |
L. S. Meadows, J. Malhotra, A. Loukas, V. Thyagarajan, K. A. Kazen-Gillespie, M. C. Koopman, S. Kriegler, L. L. Isom, and D. S. Ragsdale Functional and Biochemical Analysis of a Sodium Channel beta 1 Subunit Mutation Responsible for Generalized Epilepsy with Febrile Seizures Plus Type 1 J. Neurosci., December 15, 2002; 22(24): 10699 - 10709. [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] |
||||
![]() |
R. Chandra, C. F. Starmer, and A. O. Grant Multiple effects of KPQ deletion mutation on gating of human cardiac Na+ channels expressed in mammalian cells Am J Physiol Heart Circ Physiol, May 1, 1998; 274(5): H1643 - H1654. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Qu, L. L. Isom, R. E. Westenbroek, J. C. Rogers, T. N. Tanada, K. A. McCormick, T. Scheuer, and W. A. Catterall Modulation of Cardiac Na[IMAGE] Channel Expression in Xenopus Oocytes by beta1 Subunits J. Biol. Chem., October 27, 1995; 270(43): 25696 - 25701. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. L. Isom, T. Scheuer, A. B. Brownstein, D. S. Ragsdale, B. J. Murphy, and W. A. Catterall Functional Co-expression of the beta1 and Type IIA alpha Subunits of Sodium Channels in a Mammalian Cell Line J. Biol. Chem., February 17, 1995; 270(7): 3306 - 3312. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Isom, K. De Jongh, D. Patton, B. Reber, J Offord, H Charbonneau, K Walsh, A. Goldin, and W. Catterall Primary structure and functional expression of the beta 1 subunit of the rat brain sodium channel Science, May 8, 1992; 256(5058): 839 - 842. [Abstract] [PDF] |
||||
![]() |
D Singer, M Biel, I Lotan, V Flockerzi, F Hofmann, and N Dascal The roles of the subunits in the function of the calcium channel Science, September 27, 1991; 253(5027): 1553 - 1557. [Abstract] [PDF] |
||||
|
|