Krafte, Douglas S. and Goldin, Alan L. and Auld, Vanessa J. and Dunn, Robert J. and Davidson, Norman and Lester, Henry A. (1990) Inactivation of cloned Na channels expressed in Xenopus oocytes. Journal of General Physiology, 96 (4). pp. 689-706. ISSN 0022-1295. http://resolver.caltech.edu/CaltechAUTHORS:KRAjgp90
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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.
|Additional Information:||© 1990 by The Rockefeller University Press. Original version received 10 October 1989 and accepted version received 27 April 1990. We thank A. Gouin and W. Conley for excellent technical assistance, Dr. R.J. Leonard and Dr. I. Ahmed for helpful suggestions during the course of this work, and Dr. W. A. Catterall for comments on the manuscript. This research was supported by grants from the U.S. National Institutes of Health (NS-11756, GM-10991, and NS-26729), the Lucille P. Markey Charitable Trust, the Esther A. and Joseph Klingenstein Fund, the Multiple Sclerosis Society (Canada), the Medical Research Council (Canada), and the March of Dimes Basil O'Connor Starter Scholar Program. D.S. Krafte held a postdoctoral fellowship from the NIH. A.L. Goldin is a Lucille P. Markey Scholar.|
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|Deposited By:||Lindsay Cleary|
|Deposited On:||18 Oct 2006|
|Last Modified:||26 Dec 2012 09:05|
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