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Changes in intracellular protein expression in cortex., thalamus and hippocampus in a genetic rat model of absence epilepsy

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dc.contributor.authorOGAN, AYŞE
dc.contributor.authorsDanis, Ozkan; Demir, Serap; Gunel, Aslihan; Aker, Rezzan Gulhan; Gulcebi, Medine; Onat, Filiz; Ogan, Ayse
dc.date.accessioned2022-03-12T17:51:44Z
dc.date.available2022-03-12T17:51:44Z
dc.date.issued2011
dc.description.abstractEpilepsy is a chronic disorder characterized by repeated seizures resulting from abnormal activation of neurons in the brain. Although mutations in genes related to Na+, K+, Ca2+ channels have been defined, few studies show intracellular protein changes. We have used proteomics to investigate the expression of soluble proteins in a genetic rat model of absence epilepsy Genetic Absence Epilepsy Rats from Strasbourg (GAERS). The advantage of this technique is its high throughput quantitative and qualitative detection of all proteins with their post-translational modifications at a given time. The parietal cortex and thalamus, which are the regions responsible for the generation of absence seizures, and the hippocampus, which is not involved in this activity, were dissected from GAERS and from non-epileptic control rat brains. Proteins from each tissue sample were isolated and separated by two-dimensional gel electrophoresis. Spots that showed significantly different levels of expression between controls and GAERS were identified by nano LC-ESI-MS/MS. Identified proteins were: ATP synthase subunit delta and the 14-3-3 zeta isoform in parietal cortex; myelin basic protein and macrophage migration inhibitory factor in thalamus; and macrophage migration inhibitory factor and 0-beta 2 globulin in hippocampus. All protein expressions were up-regulated in GAERS except 0-beta globulin. These soluble proteins are related to energy generation, signal transduction, inflammatory processes and membrane conductance. These results indicate that not only membrane proteins but also cytoplasmic proteins may take place in the pathophysiology and can be therapeutic targets in absence epilepsy. (C) 2011 Elsevier Inc. All rights reserved.
dc.identifier.doi10.1016/j.brainresbull.2011.02.002
dc.identifier.eissn1873-2747
dc.identifier.issn0361-9230
dc.identifier.pubmed21310218
dc.identifier.urihttps://hdl.handle.net/11424/230328
dc.identifier.wosWOS:000289958600003
dc.language.isoeng
dc.publisherPERGAMON-ELSEVIER SCIENCE LTD
dc.relation.ispartofBRAIN RESEARCH BULLETIN
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectGAERS
dc.subjectProteomics
dc.subjectEpilepsy
dc.subjectCortex
dc.subjectThalamus
dc.subjectHippocampus
dc.subjectMIGRATION INHIBITORY FACTOR
dc.subjectMYELIN BASIC-PROTEIN
dc.subjectMITOCHONDRIAL ATP SYNTHASE
dc.subjectPOLYACRYLAMIDE GELS
dc.subjectSIGNAL-TRANSDUCTION
dc.subjectMETABOLIC-ACTIVITY
dc.subjectPROTEOMIC ANALYSIS
dc.subjectCORTICAL-NEURONS
dc.subjectWAVE DISCHARGES
dc.subjectFACTOR MIF
dc.titleChanges in intracellular protein expression in cortex., thalamus and hippocampus in a genetic rat model of absence epilepsy
dc.typearticle
dspace.entity.typePublication
local.avesis.id2c1a9195-eb79-4c3a-a030-3c60008e14f8
local.import.packageSS17
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages8
oaire.citation.endPage388
oaire.citation.issue6
oaire.citation.startPage381
oaire.citation.titleBRAIN RESEARCH BULLETIN
oaire.citation.volume84
relation.isAuthorOfPublication58db3332-a5f8-4224-a021-aeea795f52fa
relation.isAuthorOfPublication.latestForDiscovery58db3332-a5f8-4224-a021-aeea795f52fa

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