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This Article Full Text Full Text (PDF) All Versions of this Article: 554/2/439    most recent jphysiol.2003.052662v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Abegg, M. H. Articles by Gähwiler, B. H. Search for Related Content PubMed PubMed Citation Articles by Abegg, M. H. Articles by Gähwiler, B. H.

Mathias H. Abegg, Nataa Savic, Markus U. Ehrengruber, R. Anne McKinney and Beat H. Gähwiler

Brain Research Institute, University of Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland

Although epileptic seizures are characterized by excessive excitation, the role of excitatory synaptic transmission in the induction and expression of epilepsy remains unclear. Here, we show that epileptiform activity strengthens excitatory hippocampal synapses by increasing the number of functional (RS)--amino-3hydroxy-5methyl-4-isoxadepropionate (AMPA)-type glutamate receptors in CA3–CA1 synapses. This form of synaptic strengthening occludes long-term potentiation (LTP) and enhances long-term depression (LTD), processes involved in learning and memory. These changes in synaptic transmission and plasticity, which are fully blocked with N-methyl-D-aspartate (NMDA) receptor antagonists, may underlie epilepsy induction and seizure-associated memory deficits.

(Received 4 August 2003; accepted after revision 27 October 2003; first published online 31 October 2003)
Corresponding author M. H. Abegg: Brain Research Institute, University of Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland.  Email: mhabegg{at}access.unizh.ch

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