Abstracts

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 [italic]bcl-2 [/italic]family of genes during the formation of kindling model of epilepsy in rats. We examined the expression pattern of [italic]bax, bcl-2, bcl-x[sub]L[/sub], mtd [/italic]and[italic] bcl-w[/italic] both at 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 TUNEL assay. Animals have started to have epileptic discharges after the 10th day of kindling model. Recurrent subthreshold electrical stimuli induced not only epileptic foci but also the expression of [italic]bax[/italic], an inducer of apoptosis, in this time period. On the other hand, [italic]bcl-x[sub]L[/sub][/italic], 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. Our study shows differential expression of Bax and Bcl-x[sub]L[/sub] 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 has the potential to induce DNA fragmentation by altering the expression levels of Bax and Bcl-x[sub]L[/sub]. (Supported by Bilkent University Research Grant, Bilkent University Faculty Development Grant, Ege University and Tubitak (SBAG-2239).)