WWW.JNEUROSCI.ORG
-
The Journal of Neuroscience Synaptic Systems Antibody Company
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 (8)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yang, H.
Right arrow Articles by Goldowitz, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yang, H.
Right arrow Articles by Goldowitz, D.

 Previous Article  |  Next Article 

The Journal of Neuroscience, January 15, 2002, 22(2):464-470

The Community Effect and Purkinje Cell Migration in the Cerebellar Cortex: Analysis of Scrambler Chimeric Mice

Huaitao Yang, Patricia Jensen, and Dan Goldowitz

Department of Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, Tennessee 38163

The Disabled-1 protein in mouse is known to be an intercellular signaling component of the Reelin molecular pathway that subserves neuronal migration in several structures in the brain and spinal cord. The scrambler mutant mouse, which is phenotypically identical to the reeler mouse, is due to a mutation in the disabled-1 gene (Howell et al., 1997; Sheldon et al., 1997). The Purkinje cells of the cerebellum express Disabled-1 and experience a massive failure of migration in the scrambler mutant mouse (Howell et al., 1997; Sheldon et al., 1997; Gallagher et al., 1998; Rice et al., 1998). We sought to define the developmental basis of this mutation by studying the Purkinje cell population in experimental mouse aggregation chimeras using a cell marker that permitted the identification of neurons derived from the mutant lineage. We found that a genetically normal component to the environment cannot assist scrambler mutant Purkinje cells in the migratory process. However, the presence of a mutant component to the environment can cause the ectopia of wild-type Purkinje cells. There appears to be a linear relationship between the percentage of the cerebellum that is genetically mutant and the number of wild-type Purkinje cells that express a mutant phenotype. These studies point to the interplay between cell-intrinsic and cell-extrinsic properties in the migration of neurons to form laminated structures during CNS development.

Key words: cerebellum; neuronal migration; mouse chimeras; Disabled-1; Reelin; Purkinje cell

Copyright © 2002 Society for Neuroscience  0270-6474/02/222464-07$05.00/0


This article has been cited by other articles:


Home page
 Proc. Natl. Acad. Sci. USAHome page
S. M. Curristin, A. Cao, W. B. Stewart, H. Zhang, J. A. Madri, J. S. Morrow, and L. R. Ment
Disrupted synaptic development in the hypoxic newborn brain
PNAS, November 26, 2002; 99(24): 15729 - 15734.
[Abstract] [Full Text] [PDF]


-

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help
-
Copyright 2008 by Society for Neuroscience ONLINE ISSN: 1529-2401
-