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The Journal of Neuroscience, October 25, 2006, 26(43):11083-11110; doi:10.1523/JNEUROSCI.2766-06.2006

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Neurobiology of Disease
Potential New Antiepileptogenic Targets Indicated by Microarray Analysis in a Rat Model for Temporal Lobe Epilepsy

Jan A. Gorter,^1,3 Erwin A. van Vliet,^1,3 Eleonora Aronica,⁴ Timo Breit,² Han Rauwerda,² Fernando H. Lopes da Silva,¹ and Wytse J. Wadman¹

¹Center for Neuroscience and ²Micro-Array Department, Swammerdam Institute for Life Sciences, University of Amsterdam, 1098 SM, Amsterdam, The Netherlands, ³Stichting Epilepsie Instellingen Nederland, 2103 SW, Heemstede, The Netherlands, and ⁴Department of (Neuro)Pathology, Academic Medical Center, University of Amsterdam, 1105 AZ, Amsterdam, The Netherlands

Correspondence should be addressed to Dr. Jan A. Gorter, Swammerdam Institute for Life Sciences, Center for Neuroscience, University of Amsterdam, Kruislaan 320, 1098 SM, Amsterdam, The Netherlands. Email: gorter{at}science.uva.nl

To get insight into the mechanisms that may lead to progression of temporal lobe epilepsy, we investigated gene expression during epileptogenesis in the rat. RNA was obtained from three different brain regions [CA3, entorhinal cortex (EC), and cerebellum (CB)] at three different time points after electrically induced status epilepticus (SE): acute phase [group D (1 d)], latent period [group W (1 week)], and chronic epileptic period [group M (3–4 months)]. A group that was stimulated but that had not experienced SE and later epilepsy was also included (group nS). Gene expression analysis was performed using the Affymetrix Gene Chip System (RAE230A). We used GENMAPP and Gene Ontology to identify global biological trends in gene expression data. The immune response was the most prominent process changed during all three phases of epileptogenesis. Synaptic transmission was a downregulated process during the acute and latent phases. GABA receptor subunits involved in tonic inhibition were persistently downregulated. These changes were observed mostly in both CA3 and EC but not in CB. Rats that were stimulated but that did not develop spontaneous seizures later on had also some changes in gene expression, but this was not reflected in a significant change of a biological process. These data suggest that the targeting of specific genes that are involved in these biological processes may be a promising strategy to slow down or prevent the progression of epilepsy. Especially genes related to the immune response, such as complement factors, interleukins, and genes related to prostaglandin synthesis and coagulation pathway may be interesting targets.

Key words: epileptogenesis; gene ontology; immune response; CA3; entorhinal cortex; synaptic transmission; PCR; immunostaining; status epilepticus; seizure

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Received June 29, 2006; revised Sept. 4, 2006; accepted Sept. 17, 2006.

Correspondence should be addressed to Dr. Jan A. Gorter, Swammerdam Institute for Life Sciences, Center for Neuroscience, University of Amsterdam, Kruislaan 320, 1098 SM, Amsterdam, The Netherlands. Email: gorter{at}science.uva.nl

This article has been cited by other articles:

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