Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (9)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Battaglia, G.
Right arrow Articles by Setola, V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Battaglia, G.
Right arrow Articles by Setola, V.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Cerebral Cortex, Vol. 13, No. 7, 736-748, July 2003
© 2003 Oxford University Press

Neurogenesis in Cerebral Heterotopia Induced in Rats by Prenatal Methylazoxymethanol Treatment

Giorgio Battaglia, Silvia Pagliardini, Laura Saglietti, Flaminio Cattabeni1, Monica Di Luca1, Stefania Bassanini and Veronica Setola

Molecular Neuroanatomy Laboratory, Experimental Neurophysiology Department, Neurological Institute ‘C. Besta’, via Celoria 11 and , 1 Department of Pharmacological Sciences, University of Milano, Via Balzaretti 9, 20133 Milano, Italy

We have previously demonstrated that the antiproliferative agent methylazoxymethanol acetate (MAM) is able to induce in rats cerebral heterotopia that share striking similarities with those observed in human periventricular nodular heterotopia (PNH), a cerebral dysgenesis frequently observed in human patients affected by drug-resistant focal epilepsy. In this study, we investigated the time-course of neurogenesis in the cerebral heterotopia of MAM-treated rats, with the idea of understanding why PNH develop in human patients. For these goals, we analyzed the cytoarchitectural features, the time of neurogenesis and the cellular phenotype of the heterotopia, by means of BrdU immunocytochemistry and confocal immunofluorescence experiments. Our data demonstrate that the different types of heterotopia in MAM-treated rats are formed through the same altered neurogenetic process, which follows quite organized neurogenetic gradients. The MAM-induced ablation of an early wave of cortical neurons is sufficient to alter per se the migration and differentiation of subsequently generated neurons, which in turn set the base for the formation of the different heterotopic structures. The neurogenesis of MAM-induced heterotopia may explain the origin and intrinsic epileptogenicity of periventricular nodular heterotopia in human patients.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Toxicol PatholHome page
B. Bolon, R. Garman, K. Jensen, G. Krinke, B. Stuart, and An Ad Hoc Working Group of the STP Scientific and
A 'Best Practices' Approach to Neuropathologic Assessment in Developmental Neurotoxicity Testing--for Today
Toxicol Pathol, April 1, 2006; 34(3): 296 - 313.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.