The American Journal of Psychiatry
Journal Home Search Current Issue Past Issues Subscribe All APPI Journals Help Contact Us
 
Quicksearch
Advanced Search
Or Search All APPI Journals
This Article
* Full Text (PDF)
* Alert me when this article is cited
* Alert me if a correction is posted
Services
* Email this article to a Colleague
* Similar articles in this journal
* Similar articles in PubMed
* Alert me to new issues of the journal
* Add to My Articles & Searches
* Download to citation manager
* reprints & permissions
Citing Articles
* Citing Articles via Google Scholar
Google Scholar
* Articles by LOMBROSO, P. J.
* Articles by GOLDOWITZ, D.
* Search for Related Content
PubMed
* PubMed Citation
* Articles by LOMBROSO, P. J.
* Articles by GOLDOWITZ, D.
Related Collections
* Other Neuroscience
* Neurodevelopment
Am J Psychiatry 155:1660, December 1998
©Copyright 1998 American Psychiatric Association


Images In Neuroscience

Brain Development, VIII: The Reeler Mouse

Carol A. Tamminga, M.D., Editor

PAUL J. LOMBROSO, M.D.
New Haven, Conn., and DANIEL GOLDOWITZ, PH.D.
Memphis, Tenn.

Mutant mouse strains have been useful to scientists and clinicians in understanding aspects of normal CNS development. One such spontaneous mutation produces a mouse with abnormal movements and, on microscopic analysis, abnormal cortical neuronal organization. The gene responsible for this mutant mouse strain is called reeler and was recently cloned. The reeler mouse mutation causes an abnormal pattern in the layering of neurons in the neocortex and the cerebellum. Instead of the cells arranging themselves in the typical "inside-out" fashion as described by P. Rakic (Images in Neuroscience, Am J Psychiatry 1998; 155:1150–1151), they order themselves in an "outside-in" pattern (figure). As a consequence, the earliest-born neurons abnormally migrate to the surface in the reeler mouse, the next generation of neurons settle immediately below, and the final neurons form the deepest cortical layer—the exact opposite of what is normally found. These mutant mice lack a functional gene product, the protein called reelin. Reelin is highly expressed during the period of development when brain cells are migrating into the cortex. It is produced by neurons near the cortical surface, is secreted into the surrounding extracellular matrix, and is thought to guide newly formed neurons to their proper final destination. It is only then that normal synaptic connections may be established between neurons. The lack of this protein guide leaves the neuronal patterning in disarray. It is intriguing to speculate that subtle mutations in this, or related genes, may contribute to the etiology of some developmental disorders of childhood, as well as other psychiatric illnesses.



View larger version (0K):
[in this window]
[in a new window]
 

FIGURE 1



FOOTNOTES

Address reprint requests to Dr. Tamminga, Maryland Psychiatric Research Center, University of Maryland, P.O. Box 21247, Baltimore, MD 21228. Image is courtesy of Dr. Goldowitz.





This Article
* Full Text (PDF)
* Alert me when this article is cited
* Alert me if a correction is posted
Services
* Email this article to a Colleague
* Similar articles in this journal
* Similar articles in PubMed
* Alert me to new issues of the journal
* Add to My Articles & Searches
* Download to citation manager
* reprints & permissions
Citing Articles
* Citing Articles via Google Scholar
Google Scholar
* Articles by LOMBROSO, P. J.
* Articles by GOLDOWITZ, D.
* Search for Related Content
PubMed
* PubMed Citation
* Articles by LOMBROSO, P. J.
* Articles by GOLDOWITZ, D.
Related Collections
* Other Neuroscience
* Neurodevelopment


Get information about faster international access.

Privacy Policy

Copyright © 1998 American Psychiatric Association. All rights reserved.

Home | Search | Current Issue | Past Issues | Subscribe | All APPI Journals | Help | Contact Us

American Psychiatric Publishing, Inc. American Psychiatric Association
1000 Wilson Boulevard, Suite 1825, Arlington, VA 22209-3901 * 800-368-5777 * appi at psych.org