title: Altered hippocampal gene expression prior to the onset of spontaneous seizures in the rat post-status epilepticus model.
abstract: Neuronal loss, gliosis and axonal sprouting in the hippocampal formation are characteristics of the syndrome of mesial temporal sclerosis (MTS). In the post-status epilepticus (SE) rat model of spontaneous seizures these features of the MTS syndrome can be reproduced. To get a global view of the changes in gene expression in the hippocampus we applied serial analysis of gene expression (SAGE) during the early phase of epileptogenesis (latent period), prior to the onset of the first spontaneous seizure. A total of 10 000 SAGE tags were analyzed per experimental group, resulting in 5053 (SE) and 5918 (control group) unique tags (genes), each representing a specific mRNA transcript. Of these, 92 genes were differentially expressed in the hippocampus of post-SE rats in comparison to controls. These genes appeared to be mainly associated with ribosomal proteins, protein processing, axonal growth and glial proliferation proteins. Verification of two of the differentially expressed genes by in situ hybridization confirmed the changes found by SAGE. Histological analysis of hippocampal sections obtained 8 days after SE showed extensive cell loss, mossy fibre sprouting and gliosis in hippocampal sub regions. This study identifies new high-abundant genes that may play an important role in post-SE epileptogenesis.
authors.affiliation: Swammerdam Institute for Life Sciences (SILS), Section Neurobiology, University of Amsterdam, Kruislaan 320, 1098 SM Amsterdam, The Netherlands.
authors.forename: H
authors.initials: H
authors.lastname: Hendriksen
authors.forename: N A
authors.initials: NA
authors.lastname: Datson
authors.forename: W E
authors.initials: WE
authors.lastname: Ghijsen
authors.forename: E A
authors.initials: EA
authors.lastname: van Vliet
authors.forename: F H
authors.initials: FH
authors.lastname: da Silva
authors.forename: J A
authors.initials: JA
authors.lastname: Gorter
authors.forename: E
authors.initials: E
authors.lastname: Vreugdenhil
mesh_terms: D000818:Animals; D001483:Base Sequence / Q000235:genetics; D051152:Clusterin; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000235:genetics; D004569:Electroencephalography; D004827:Epilepsy / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D004833:Epilepsy, Temporal Lobe / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D005786:Gene Expression Regulation / Q000502:physiology*; D005819:Genetic Markers / Q000235:genetics; D006023:Glycoproteins / Q000235:genetics / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D007150:Immunohistochemistry; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D018832:Molecular Chaperones / Q000235:genetics / Q000378:metabolism; D009410:Nerve Degeneration / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D009416:Nerve Regeneration / Q000235:genetics; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013226:Status Epilepticus / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D013997:Time Factors; D014158:Transcription, Genetic / Q000235:genetics; D014404:Tubulin / Q000235:genetics / Q000378:metabolism; D015854:Up-Regulation / Q000235:genetics
chemical_list: D051152:Clusterin; D005819:Genetic Markers; D006023:Glycoproteins; D018832:Molecular Chaperones; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger; D014404:Tubulin