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The role of bcl-2 family of genes during kindling

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dc.contributor.author Akcali, K.C.
dc.contributor.author Şahiner, Melike
dc.contributor.author Şahiner, Türker
dc.date.accessioned 2019-08-16T11:39:02Z
dc.date.available 2019-08-16T11:39:02Z
dc.date.issued 2005
dc.identifier.issn 00139580 (ISSN)
dc.identifier.uri http://acikerisim.pau.edu.tr:8080/xmlui/handle/11499/4929
dc.description.abstract Purpose: 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.
dc.language.iso English
dc.relation.isversionof 10.1111/j.0013-9580.2005.13904.x
dc.rights info:eu-repo/semantics/openAccess
dc.subject Apoptosis
dc.subject Bcl-2 family of genes
dc.subject Epilepsy
dc.subject Kindling
dc.subject Rat
dc.subject brain protein
dc.subject DNA fragment
dc.subject DNA nucleotidylexotransferase
dc.subject membrane protein
dc.subject messenger RNA
dc.subject protein Bax
dc.subject protein bcl 2
dc.subject protein bcl w
dc.subject protein bcl xl
dc.subject protein mtd
dc.subject unclassified drug
dc.subject animal experiment
dc.subject animal model
dc.subject apoptosis
dc.subject article
dc.subject controlled study
dc.subject electrostimulation
dc.subject epilepsy
dc.subject epileptic discharge
dc.subject epileptic focus
dc.subject hippocampus
dc.subject kindling
dc.subject male
dc.subject nerve cell membrane potential
dc.subject nonhuman
dc.subject priority journal
dc.subject protein expression
dc.subject rat
dc.subject Animals
dc.subject bcl-2-Associated X Protein
dc.subject Disease Models, Animal
dc.subject DNA Fragmentation
dc.subject Electric Stimulation
dc.subject Electrodes, Implanted
dc.subject Epilepsy, Temporal Lobe
dc.subject Gene Expression
dc.subject Genes, bcl-2
dc.subject Hippocampus
dc.subject Immunohistochemistry
dc.subject In Situ Nick-End Labeling
dc.subject Kindling, Neurologic
dc.subject Male
dc.subject Proto-Oncogene Proteins c-bcl-2
dc.subject Rats
dc.subject Rats, Sprague-Dawley
dc.subject RNA, Messenger
dc.title The role of bcl-2 family of genes during kindling
dc.type Article
dc.relation.journal Epilepsia
dc.contributor.authorID 0000-0002-2009-6949
dc.identifier.volume 46
dc.identifier.issue 2
dc.identifier.startpage 217
dc.identifier.endpage 223
dc.relation.publicationCategory Ulusal özet bildiri
dc.identifier.index Scopus
dc.identifier.index WOS


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