JN AJP: Advances in Physiology Education
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Neurophysiol 92: 672, 2004; doi:10.1152/jn.00313.2004
0022-3077/04 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
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
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 Google Scholar
Google Scholar
Right arrow Articles by Colbert, C. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Colbert, C. M.

EDITORIAL FOCUS

Is Resurgent Na+ Current an Alpha-Subunit-Specific Property? Maybe Not. Focus on "Sodium Currents in Subthalamic Nucleus Neurons From Nav1.6-Null Mice"

During the past quarter century Na+ channels have slowly but steadily revealed their kinetic complexity and diversity. Far beyond the one-trick pony of the Hodgkin-Huxley Na+ channel that rapidly activates and inactivates to produce action potentials, Na+ channels continue to display an ever-increasing variety of kinetic properties such as persistence, slow-inactivation, and most recently "resurgence." Resurgent current flows when an open-channel block is relieved by rapid repolarization from positive potentials. Resurgent current immediately after an action potential may promote firing of a subsequent spike not only because of the inward current itself, but also because the flow of this current is associated with a more rapid recovery from inactivation (Raman and Bean 2001Go). Resurgent currents were first described in Purkinje cells where they improve high-frequency firing (Raman and Bean 1997Go). More recently, resurgent currents have also been implicated in rhythmic firing of neurons in the subthalamic nucleus, an area gaining importance in the treatment of end-stage Parkinson's syndromes (Do and Bean 2003Go). Few neurons throughout the brain, however, are known to display resurgent currents, suggesting that these currents are carried by a select subset of Na+ channels. Compelling evidence that this subset corresponds to one particular Na+ channel subunit is the finding that Purkinje cells lacking Nav1.6 alpha subunits (med mutant) do not display resurgent currents. However, under conditions of artificially induced slowing of inactivation by beta-pompilidotoxin, the remaining Na+ channels could be made to produce a resurgent current (Grieco and Raman 2004Go). The report by Do and Bean (this issue, p. 726–733) sheds further light on this story. By identifying resurgent current in subthalamic nucleus neurons from mice lacking the Nav1.6 alpha subunits, they demonstrate that resurgent current is not a property unique to Nav1.6 subunits. Do and Bean's findings suggest instead that some form of modulation or an association with an auxiliary subunit, rather than the specific alpha subunit, is critical for the production of resurgent current. Such an association would need to produce a secondary inactivation to compete with classical fast inactivation. Whatever the nature of this putative element, different classes of neurons may rely on different Na+ channel alpha-subunits to produce resurgent currents. Resurgent currents may indeed represent a more ubiquitous determinant of cell-specific firing than we now appreciate.

Costa M. Colbert

Department of Biology and Biochemistry, University of Houston, Houston, Texas 77204-5513

Address for reprint requests and other correspondence: Dept. of Biology and Biochemistry, University of Houston, 4800 Calhoun Rd., Houston TX, 77204-5513 (E-mail: ccolbert{at}uh.edu).

REFERENCES

Do MT and Bean BP. Sodium currents in subthalamic nucleus neurons from Nav1.6-null mice. J Neurophysiol 92: 726–733, 2004.[Abstract/Free Full Text]

Do MT and Bean BP. Subthreshold sodium currents and pacemaking of subthalamic neurons: modulation by slow inactivation. Neuron 39: 109–120, 2003.[CrossRef][Web of Science][Medline]

Grieco TM and Raman IM. Production of resurgent current in NaV1.6-null Purkinje neurons by slowing sodium channel inactivation with beta-pompilidotoxin. J Neurosci 24: 35–42, 2004.[Abstract/Free Full Text]

Raman IM and Bean BP. Inactivation and recovery of sodium currents in cerebellar Purkinje neurons: evidence for two mechanisms. Biophys J 80: 729–737, 2001.[Web of Science][Medline]

Raman IM and Bean BP. Resurgent sodium current and action potential formation in dissociated cerebellar Purkinje neurons. J Neurosci 17: 4517–4526, 1997.[Abstract/Free Full Text]





This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
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
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 Google Scholar
Google Scholar
Right arrow Articles by Colbert, C. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Colbert, C. M.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2004 by the The American Physiological Society.