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Brain Advance Access originally published online on January 6, 2006
Brain 2006 129(3):625-641; 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

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

Sarah Jamali1, Fabrice Bartolomei2,3, Andrée Robaglia-Schlupp1,6, Annick Massacrier1, Jean-Claude Peragut4, Jean Régis4, Henri Dufour5, Rivka Ravid9, Patrice Roll1, Sandrine Pereira1, Barbara Royer1, Nathalie Roeckel-Trevisiol1, Marc Fontaine8, Maxime Guye2,3, José Boucraut7, Patrick Chauvel2,3, Pierre Cau1,6 and Pierre Szepetowski1

1 INSERM UMR 491 and 2 INSERM EMI 9926, Université de la Méditerranée, 3 Service de Neurophysiologie Clinique, 4 Service de Neurochirurgie Fonctionnelle et Stéréotaxie, 5 Service de Neurochirurgie, Hôpital de la Timone, 6 Laboratoire de Biologie Cellulaire and 7 Laboratoire d'Immunologie, Hôpital de la Conception, Marseille, 8 INSERM U413, Université de Rouen, Rouen, France and 9 Netherlands Brain Bank, Amsterdam, The Netherlands

Correspondence to: Dr P. Szepetowski, Inserm U491, ‘Genetics of Human Epilepsies’ Group, Faculté de Médecine de la Timone, 27 Boulevard J Moulin, 13385 Marseille Cedex 5, France E-mail: szepetowski{at}medecine.univ-mrs.fr

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.

Key Words: epilepsy; entorhinal cortex; microarray; NPY1R; complement

Abbreviations: EC = entorhinal cortex; LTC = lateral temporal neocortex; MAC = membrane attack complex; MTLE = mesial temporal lobe epilepsies; NPY1R = neuropeptide Y receptor type 1

Received July 5, 2005. Revised November 21, 2005. Accepted November 29, 2005.


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