JN Add DOIs to your references at manuscript stage!
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Neurophysiol 96: 109-118, 2006. First published February 8, 2006; doi:10.1152/jn.01369.2005
0022-3077/06 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
96/1/109    most recent
01369.2005v1
Right arrow Alert me when this article is cited
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 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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (5)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wang, Y.-C.
Right arrow Articles by Huang, R.-C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wang, Y.-C.
Right arrow Articles by Huang, R.-C.

Effects of Sodium Pump Activity on Spontaneous Firing in Neurons of the Rat Suprachiasmatic Nucleus

Yi-Chi Wang and Rong-Chi Huang

Department of Physiology and Pharmacology, Chang Gung University School of Medicine, Tao-Yuan, Taiwan

Submitted 27 December 2005; accepted in final form 7 February 2006

Cell-attached and whole cell recording techniques were used to study the effects of electrogenic sodium pump on the excitability of rat suprachiasmatic nucleus (SCN) neurons. Blocking the sodium pump with the cardiac steroid strophanthidin or zero K+ increased the spontaneous firing of SCN neurons to different degrees with different recording modes, whereas turning the sodium pump into a nonselective cation channel with the marine toxin palytoxin invariably increased the spontaneous firing to the point of total blockade. Current-clamp recordings indicated that strophanthidin increased the rate of membrane depolarization and reduced the peak afterhyperpolarization potential (AHP), whereas zero K+ also increased the rate of depolarization, but enhanced the peak AHP. The dual effect of zero K+ was reflected by the biphasic time course of voltage responses to zero K+: an inhibitory phase with enhanced peak AHP and slower firing, followed by a delayed excitatory phase with faster rate of membrane depolarization and faster firing. In the presence of strophanthidin to block the sodium pump, zero K+ consistently decreased firing by enhancing the peak AHP. Repetitive applications of K+-free solution gradually turned the biphasic inhibitory-followed-by-excitatory voltage response into a monophasic inhibitory response in cells recorded with the whole cell (but not the cell-attached) mode, suggesting rundown of sodium pump activity. Taken together, the results suggest that spontaneous firing of SCN neurons is regulated by sodium pump activity as well as the AHP, and that sodium pump activity is modulated by intracellular soluble substances subject to rundown under the whole cell conditions.


Address for reprint requests and other correspondence: R.-C. Huang, Department of Physiology and Pharmacology, Chang Gung University School of Medicine, 259 Wen-Hwa 1st Road, Kwei-San, Tao-Yuan, Taiwan (E-mail: rongchi{at}mail.cgu.edu.tw)




This article has been cited by other articles:


Home page
J. Physiol.Home page
C.-H. Chen, Y.-T. Hsu, C.-C. Chen, and R.-C. Huang
Acid-sensing ion channels in neurones of the rat suprachiasmatic nucleus
J. Physiol., April 15, 2009; 587(8): 1727 - 1737.
[Abstract] [Full Text] [PDF]


Home page
J. Physiol.Home page
M. V. Podda, M. D'Ascenzo, L. Leone, R. Piacentini, G. B. Azzena, and C. Grassi
Functional role of cyclic nucleotide-gated channels in rat medial vestibular nucleus neurons
J. Physiol., February 1, 2008; 586(3): 803 - 815.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2006 by the The American Physiological Society.