The role of bcl-2 family of genes during kindling

Simple item page
dc.citation.epage223en_US
dc.citation.issueNumber2en_US
dc.citation.spage217en_US
dc.citation.volumeNumber46en_US
dc.contributor.authorAkcali, K. C.en_US
dc.contributor.authorSahiner, M.en_US
dc.contributor.authorSahiner, T.en_US
dc.date.accessioned2016-02-08T10:24:18Z
dc.date.available2016-02-08T10:24:18Z
dc.date.issued2005en_US
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.description.abstractPurpose: Several experimental models of human temporal lobe epilepsy have shown that apoptotic death of neurons is an important part of this degenerative disease. However, the role of apoptotic regulators is not clear during the epileptogenesis. Therefore we investigated the expression pattern of bcl-2 family of genes during the formation of kindling model of epilepsy in rats. Methods: We examined the expression pattern of bax, bcl-2, bcl-xL, mtd, and bcl-w both at messenger RNA (mRNA) and protein level in the brain tissues during the formation of epilepsy with kindling model in adult rats, which has been the most acceptable form of experimental model of human epilepsy. We also assessed the onset of DNA fragmentation by using the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay. Results: Animals have started to have epileptic discharges after day 10 of kindling model. Recurrent subthreshold electrical stimuli induced not only epileptic foci but also the expression of box, an inducer of apoptosis, in this time period. Conversely, bcl-xL, which is an inhibitor of apoptosis, had an opposite pattern of expression both at mRNA and protein level during the formation of epilepsy. We did not observe DNA fragmentation by TUNEL staining. Conclusions: Our study shows differential expression of Bax and Bcl-x L at the CA1 region during the formation of hippocampal kindling model. The absence of DNA fragmentation during this period suggests that epileptic changes in neurons have the potential to induce DNA fragmentation by altering the expression levels of Bax and Bcl-xL.en_US
dc.description.provenanceMade available in DSpace on 2016-02-08T10:24:18Z (GMT). No. of bitstreams: 1 bilkent-research-paper.pdf: 70227 bytes, checksum: 26e812c6f5156f83f0e77b261a471b5a (MD5) Previous issue date: 2005en
dc.identifier.doi10.1111/j.0013-9580.2005.13904.xen_US
dc.identifier.issn0013-9580
dc.identifier.urihttp://hdl.handle.net/11693/24113
dc.language.isoEnglishen_US
dc.publisherBlackwell Publicationen_US
dc.relation.isversionofhttp://dx.doi.org/10.1111/j.0013-9580.2005.13904.xen_US
dc.source.titleEpilepsiaen_US
dc.subjectApoptosisen_US
dc.subjectBcl-2 family of genesen_US
dc.subjectEpilepsyen_US
dc.subjectKindlingen_US
dc.subjectRaten_US
dc.subjectBrain proteinen_US
dc.subjectDNA fragmenten_US
dc.subjectDNA nucleotidylexotransferaseen_US
dc.subjectMembrane proteinen_US
dc.titleThe role of bcl-2 family of genes during kindlingen_US
dc.typeArticleen_US

Files

Original bundle
Now showing 1 - 1 of 1
Thumbnail Image
Name:
The role of bcl-2 family of genes during kindling.pdf
Size:
229.81 KB
Format:
Adobe Portable Document Format
Description:
Full printable version
Download

Collections

Scholarly Publications - Molecular Biology and Genetics