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Brain Advance Access published online on January 6, 2006
Brain, doi:10.1093/brain/awl001
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© The Author (2006). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received July 5, 2005
Revised November 21, 2005
Accepted November 29, 2005

Article

Large-scale expression study of human mesial temporal lobe epilepsy: evidence for dysregulation of the neurotransmission and complement systems in the entorhinal cortex

Sarah Jamali 1, Fabrice Bartolomei 2, Andrée Robaglia-Schlupp 3, Annick Massacrier 1, Jean-Claude Peragut 4, Jean Régis 4, Henri Dufour 5, Rivka Ravid 6, Patrice Roll 1, Sandrine Pereira 1, Barbara Royer 1, Nathalie Roeckel-Trevisiol 1, Marc Fontaine 7, Maxime Guye 2, José Boucraut 8, Patrick Chauvel 2, Pierre Cau 3, and Pierre Szepetowski 1 *

1 INSERM UMR 491, Université de la Méditerranée, Marseille, France
2 INSERM EMI 9926, Université de la Méditerranée, Marseille, France; Service de Neurophysiologie Clinique, Hôpital de la Timone, Marseille, France
3 INSERM UMR 491, Université de la Méditerranée, Marseille, France; Laboratoire de Biologie Cellulaire, Hôpital de la Conception, Marseille, France
4 Service de Neurochirurgie Fonctionnelle et Stéréotaxie, Hôpital de la Timone, Marseille, France
5 Service de Neurochirurgie, Hôpital de la Timone, Marseille, France
6 Netherlands Brain Bank, Amsterdam, The Netherlands
7 INSERM U413, Université de Rouen, Rouen, France
8 Laboratoire d'Immunologie, Hôpital de la Conception, Marseille, France

* To whom correspondence should be addressed.
Pierre Szepetowski, E-mail: szepetowski{at}medecine.univ-mrs.fr


  Abstract

Human mesial temporal lobe epilepsies (MTLE) are the most frequent form of partial epilepsies and display frequent pharmacoresistance. The molecular alterations underlying human MTLE remain poorly understood. A two-step transcriptional analysis consisting in cDNA microarray experiments followed by quantitative RT-PCR validations was performed. Because the entorhinal cortex (EC) plays an important role in the pathophysiology of the MTLE and usually discloses no detectable or little cell loss, resected EC and each corresponding lateral temporal neocortex (LTC) of MTLE patients were used as the source of disease-associated and control RNAs, respectively. Six genes encoding (i) a serotonin receptor (HTR2A) and a neuropeptide Y receptor type 1 (NPY1R), (ii) a protein (FHL2) associating with the KCNE1 (minK) potassium channel subunit and with presenilin-2 and (iii) three immune system-related proteins (C3, HLA-DR-{gamma} and CD99), were found consistently downregulated or upregulated in the EC of MTLE patients as compared with non-epileptic autopsy controls. Quantitative western blot analyses confirmed decreased expression of NPY1R in all eight MTLE patients tested. Immunohistochemistry experiments revealed the existence of a perivascular infiltration of C3 positive leucocytes and/or detected membrane attack complexes on a subset of neurons, within the EC of nine out of eleven MTLE patients. To summarize, a large-scale microarray expression study on the EC of MTLE patients led to the identification of six candidate genes for human MTLE pathophysiology. Altered expression of NPY1R and C3 was also demonstrated at the protein level. Overall, our data indicate that local dysregulation of the neurotransmission and complement systems in the EC is a frequent event in human MTLE.

Keywords: epilepsy; entorhinal cortex; microarray; NPY1R; complement.
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