JCB logo
MBoC5 from Garland Science
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

Published online 30 December 2002. doi:10.1083/jcb1601rr5
This Article
Right arrow PDF (Full Text)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wells, W. A.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Wells, W. A.
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, 0021-9525/2003/1/9-a $5.00
The Journal of Cell Biology, Volume 160, Number 1, 9-a-9


Research Roundup

A trigger for myelination


Oligodendrocytes (arrows) are activated by signals from active neurons (center).

Fields/Elsevier

Some cells can induce the production of their own protective blanket. The signal comes from active neurons in the central nervous system (CNS), and triggers the differentiation of oligodendrocyte precursor cells (OPCs)—thus yielding the cells that cover the neurons with a protective sheath of myelin. Now, Beth Stevens, Douglas Fields, and colleagues (National Institutes of Health, Bethesda, MD) have shown that the neurons accomplish this task by releasing a simple metabolite, adenosine.

The finding could be critical for possible stem cell treatments for the myelinating disease multiple sclerosis. "The problem [with stem cell treatments] is not getting the stem cells; the problem is getting the cells to differentiate at the right stage," says Fields. Adenosine looks like a promising stop signal for OPCs. And, as a further enticement, Fields showed that a brief exposure to adenosine might be enough to set cells on the right path.

Fields added a wide variety of biomolecules to OPCs and found that adenosine alone could reduce proliferation and induce everything from differentiation markers to a differentiated morphology and myelination. Adenosine receptor antagonists, meanwhile, prevented the changes in OPC proliferation and morphology normally caused by active neurons.

These results contrasted with the group's earlier findings with Schwann cells, which provide myelination for the peripheral nervous system (PNS). For Schwann cells it is ATP that is active but with an opposite effect: the ATP arrests maturation. This may give the PNS axons time to mature before they are surrounded by myelin.

The regulation of the two systems will take some time to decipher. ATP and adenosine not only have different effects on OPCs and Schwann cells, but one metabolite can be converted to the other via extracellular enzymes. Fields thinks the decoding effort will be worthwhile. "As neuroscientists we are all focused on rapid communication," he says, "but all cells communicate, and this is one of the most ancient systems." {blacksquare}

Reference:

Stevens, B., et al. 2002. Neuron. 36:855–868.[CrossRef][Medline]



William A. Wells

wellsw{at}rockefeller.edu


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?



This Article
Right arrow PDF (Full Text)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wells, W. A.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Wells, W. A.
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?


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