Skip Navigation


Cerebral Cortex Advance Access first published online on April 27, 2004
This version published online on July 6, 2004
Cerebral Cortex, doi:10.1093/cercor/bhh067
© 2004 by Oxford University Press
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
14/10/1081    most recent
bhh067v2
bhh067v1
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 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 arrowRequest Permissions
Google Scholar
Right arrow Articles by Peters, O.
Right arrow Articles by Witte, O. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Peters, O.
Right arrow Articles by Witte, O. W.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Article

Impaired Synaptic Plasticity in the Surround of Perinatally Aquired Dysplasia in Rat Cerebral Cortex

Oliver Peters 1*, Christoph Redecker 2, Georg Hagemann 2, Claus Bruehl 2, Heiko J. Luhmann 3, Otto W. Witte 2

1 Department of Psychiatry and Psychotherapy, Charité - University Medicine Berlin, Benjamin Franklin Campus, Eschenallee 3, D-14050 Berlin, Germany
2 Department of Neurology, Friedrich-Schiller University, Philosophenweg 3, D-07740 Jena, Germany
3 Institute of Physiology and Pathophysiology, Johannes-Gutenberg University, Duesbergweg 6, D-55128 Mainz, Germany

* To whom correspondence should be addressed. E-mail: oliver.peters{at}charite.de.


  Abstract

Freeze-lesion induced neocortical dysplasias in rats mimic numerous aspects of human polymicrogyria and are used as a model for the study of developmental migration disorders. Since memory tests have demonstrated learning deficits in rodents with neocortical malformations, we investigated the expression and properties of long-term potentiation (LTP) in neocortical slices from adult freeze-lesioned and control rats. Field potentials, recorded in layer II/III at a distance of 2-3 mm lateral to perinatally induced microgyri, were strongly enhanced following theta-burst stimulation in layer VI (amplitude: 174 ± 4%) compared to controls (110 ± 2%). In contrast, in layer IV of the freeze-lesioned cortex LTP could not reliably be induced. Histochemical analysis, performed to elucidate the cellular basis of the impaired plasticity, revealed diminished amounts of the GABAA-receptor subunit {gamma}2 in the paramicrogyral zone, likely representing a diminished GABA-ergic filter, which is thought to prevent LTP induced in layer VI under normal conditions. Cytochrome-oxidase staining after electrophysiological examination disclosed that LTP in layer IV of the freeze-lesioned cortex could only be elicited, when stimulation was applied within a preserved barrel cortex. Our study provides evidence that focal cryolesions during cortical development cause an impaired synaptic plasticity that may underlie learning disabilities.

Keywords: developmental migration disorder, learning disabilities, long-term potentiation, neocortical malformation, polymicrogyria.
This version contains the details for Mountcastle (1997) in the reference list
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




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.