WWW.JNEUROSCI.ORG
-
The Journal of Neuroscience MBF Bioscience Autoneuron
 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 Koszowski, A. G.
Right arrow Articles by Levinson, S. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Koszowski, A. G.
Right arrow Articles by Levinson, S. R.

 Previous Article  |  Next Article 

The Journal of Neuroscience, August 1, 1998, 18(15):5859-5868

The Effect of the Mouse Mutation Claw Paw on Myelination and Nodal Frequency in Sciatic Nerves

Adam G. Koszowski1, Geoffrey C. Owens2, 3, and S. Rock Levinson1, 3

Departments of 1 Physiology and Biophysics and 2 Biochemistry and Molecular Genetics and 3 Program in Neuroscience, University of Colorado Health Sciences Center, Denver, Colorado 80262

Despite the biophysical and clinical importance of differentiating nodal and internodal axolemma, very little is known about the process. We chose to study myelination and node of Ranvier formation in the hypomyelinating mouse mutant claw paw (clp). The phenotype of clp is delayed myelination in the peripheral nervous system. The specific defect is unknown but is thought to arise from a breakdown in the complex signaling mechanism between axon and Schwann cell. Myelination was assessed in sciatic nerve cross sections from adult and postnatal day 14 (P14) heterozygous and homozygous clp mice. Antibodies to P0, myelin-associated glycoprotein (MAG), and neural cell adhesion molecule were used to assess the stage of myelination. P14 homozygous clp mice showed an atypical staining pattern of immature myelin, which resolved into a relatively normal pattern by adulthood. Sodium channel clustering and node of Ranvier frequency were studied in whole-mount sciatic nerves with sodium channel and MAG antibodies. P14 homozygous clp nerves again showed an atypical, immature pattern with diffuse sodium channel clusters suggesting nodal formation was delayed. In the adult, homozygous clp sciatic nerves displayed dramatically shortened internodal distances. The data from this study support the hypotheses that node of Ranvier formation begins with the onset of myelination and that the number and location of nodes of Ranvier in the sciatic nerve are determined by myelinating Schwann cells.

Key words: internodal length; claw paw; sciatic nerve; node of Ranvier; sodium channel; immunocytochemistry; MAG; NCAM; P0


Copyright © 1998 Society for Neuroscience  0270-6474/98/18155859-10$05.00/0


This article has been cited by other articles:


Home page
J. Neurosci.Home page
M. N. Rasband, E. Peles, J. S. Trimmer, S. R. Levinson, S. E. Lux, and P. Shrager
Dependence of Nodal Sodium Channel Clustering on Paranodal Axoglial Contact in the Developing CNS
J. Neurosci., September 1, 1999; 19(17): 7516 - 7528.
[Abstract] [Full Text] [PDF]



-

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help

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