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Cerebral Cortex Advance Access published online on April 27, 2004
Cerebral Cortex, doi:10.1093/cercor/bhh067
© 2004 by Oxford University Press
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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.

Key Words: developmental migration disorder, learning disabilities, long-term potentiation, neocortical malformation, polymicrogyria


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