JCB logo
Avanti Polar Lipids
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published online 23 September 2002. doi:10.1083/jcb.200204010
This Article
Right arrow Full Text
Right arrow PDF (Full Text)
Right arrow PPT slides of all figures
Right arrow Correction (v159,p707)
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Storey, N.
Right arrow Articles by Bevan, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Storey, N.
Right arrow Articles by Bevan, S.
Related Collections
Right arrowRelated Article
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
© The Rockefeller University Press, 0021-9525/2002/9/1251 $5.00
The Journal of Cell Biology, Volume 158, Number 7, September 30, 2002 1251-1262

Article

 Selective internalization of sodium channels in rat dorsal root ganglion neurons infected with herpes simplex virus-1

Nina Storey1, David Latchman2 and Stuart Bevan1

1 Novartis Institute for Medical Sciences, London WC1E 6BS, UK
2 Windeyer Department of Molecular Pathology, University College London Medical School, The Windeyer Institute of Medical Sciences, London W1P 6DB, UK

Address correspondence to Nina Storey at her present address, National Institute of Environmental Health Sciences, 111 Alexander Dr., PO Box 12233, Mail Drop F205, Research Triangle Park, NC 27709. Tel.: (919) 541-0287. Fax: (919) 541-1431. E-mail: storey{at}niehs.nih.gov

The neurotropic virus, herpes simplex type 1 (HSV-1), inhibits the excitability of peripheral mammalian neurons, but the molecular mechanism of this effect has not been identified. Here, we use voltage-clamp measurement of ionic currents and an antibody against sodium channels to show that loss of excitability results from the selective, precipitous, and complete internalization of voltage-activated sodium channel proteins from the plasma membrane of neurons dissociated from rat dorsal root ganglion. The internalization process requires viral protein synthesis but not viral encapsulation, and does not alter the density of voltage-activated calcium or potassium channels. However, internalization is blocked completely when viruses lack the neurovirulence factor, infected cell protein 34.5, or when endocytosis is inhibited with bafilomycin A1 or chloroquine. Although it has been recognized for many years that viruses cause cell pathology by interfering with signal transduction pathways, this is the first example of viral pathology resulting from selective internalization of an integral membrane protein. In studying the HSV-induced redistribution of sodium channels, we have uncovered a previously unknown pathway for the rapid and dynamic control of excitability in sensory neurons by internalization of sodium channels.

Key Words: voltage-gated sodium channels; sensory neurons; sodium channel regulation; calcium channels; potassium channels


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?

Related Article

Herpes spoils excitement
Alan W. Dove
J. Cell Biol. 2002 158: 1153. [Full Text] [PDF]



This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents