1. ¹INSERM U 666, Faculty of Medicine, Strasbourg, France
2. ²American Memorial Hospital, Centre Hospitalier Universitaire, Reims, France
3. ³Immunopharmacology (EA2070) IFR 53, University of Reims, Reims, France

Correspondence: Dr A Nehlig, INSERM U 666, Faculty of Medicine, 11 rue Humann, 67085 Strasbourg Cedex, France. E-mail: nehlig@neurochem.u-strasbg.fr

⁴These authors contributed equally to this work.

Received 22 October 2005; Revised 26 January 2006; Accepted 30 January 2006; Published online 15 March 2006.

Abstract

Glutamate excitotoxicity has been involved in the pathophysiology of epilepsy. Normal functioning of glutamate transporters clears the synaptically released glutamate to prevent excitotoxic neuronal death. Using densitometric immunohistochemical analysis, we examined the temporal expression of the neuronal glutamate transporter (EAAC1) in the lithium-pilocarpine rat model of temporal lobe epilepsy. During the acute period of lithium-pilocarpine-induced status epilepticus, EAAC1 transporter expression increased in the pyramidal neurons of cornus ammonis (CA)1, CA2 and CA3 (fields of the hippocampus), in dentate gyrus (DG) granule cells and in olfactory tubercle (Tu). During the latent period, EAAC1 expression was strongly expressed in the DG granular and molecular layers, Tu, cerebral cortex and septum, and went back to control levels in CA1, CA2 and CA3 layers. The overexpression of EAAC1 occurred mainly in structures prone to develop Fluoro-Jade-B-positive degenerating neurons. It is, however, not clear to what extent the overexpression of EAAC1 contributes to epileptogenesis and in which area it may represent a preventive or compensatory or response to injury.