WWW.JNEUROSCI.ORG
-
The Journal of Neuroscience Discover www.zeiss.de/functionality
 QUICK SEARCH:   [advanced]


     
-


HOME
  |  
SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

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 ISI 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 ISI Web of Science (7)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kuo, C.-C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kuo, C.-C.
Right arrowPubmed/NCBI databases
*Gene*GEO Profiles
*HomoloGene*UniGene
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*POTASSIUM
*SODIUM

 Previous Article  |  Next Article 

Volume 17, Number 10, Issue of May 15, 1997 pp. 3436-3444
Copyright ©1997 Society for Neuroscience

Deactivation Retards Recovery from Inactivation in Shaker K+ Channels

Received Jan. 3, 1997; revised Feb. 24, 1997; accepted Feb. 27, 1997.

Chung-Chin Kuo

Department of Physiology, National Taiwan University College of Medicine, and Department of Neurology, National Taiwan University Hospital, Taipei 100, Taiwan, Republic of China

In Na+ channels, recovery from inactivation begins with a delay, followed by an exponential course, and hyperpolarization shortens the delay as well as hastens the entire exponential phase. These findings have been taken to indicate that Na+ channels must deactivate to recover from inactivation, and deactivation facilitates the unbinding of the inactivating particle. In contrast, it is demonstrated in this study that recovery from inactivation in Shaker K+ channels begins with no delay on repolarization. Moreover, hyperpolarization hastens only the initial phase (fast component) of recovery yet retards the later phases of recovery by increasing the proportion of slow components. The time course of slow inward "tail" K+ currents, which presumably result from the open state(s) traversed by the recovering inactivated channel, always matches the fast, but not the slow, components of recovery, suggesting that the fast and the slow components primarily correspond to recovery via the open state (unblocking of the inactivating particle before channel deactivation) and via the closed state (deactivation before unblocking), respectively. Besides, changing external K+ concentration effectively alters the absolute value of the initial recovery speed, but not its voltage dependence. It seems that Shaker K+ channel deactivation hinders, rather than facilitates, the unbinding of the inactivating particle and therefore retards recovery from inactivation, whereas external K+ may enhance unbinding of the inactivating particle by binding to a site located near the external entrance of the pore.

Key words: two-electrode voltage clamp; Shaker K+ channel; deactivation; ball and chain model of inactivation; recovery from inactivation; K+ ion binding site




This article has been cited by other articles:


Home page
J. Pharmacol. Exp. Ther.Home page
S.-B. Yang, F. Major, L. F. Tietze, and M. Rupnik
Block of Delayed-Rectifier Potassium Channels by Reduced Haloperidol and Related Compounds in Mouse Cortical Neurons
J. Pharmacol. Exp. Ther., October 1, 2005; 315(1): 352 - 362.
[Abstract] [Full Text] [PDF]


Home page
J. Neurosci.Home page
C.-C. Kuo and S. Yang
Recovery from Inactivation of T-Type Ca2+ Channels in Rat Thalamic Neurons
J. Neurosci., March 15, 2001; 21(6): 1884 - 1892.
[Abstract] [Full Text] [PDF]


Home page
J. Neurosci.Home page
C.-C. Kuo and S.-Y. Liao
Facilitation of Recovery from Inactivation by External Na+ and Location of the Activation Gate in Neuronal Na+ Channels
J. Neurosci., August 1, 2000; 20(15): 5639 - 5646.
[Abstract] [Full Text] [PDF]



-

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help

-
Copyright 2008 by Society for Neuroscience ONLINE ISSN: 1529-2401
-