Hippocampal and cortical bax, Bcl-2 and cytochrome-c gene expression analysis in different experimental epilepsy models in rats

Purpose: This study aims to determine the expression profiles of the major apoptotic pathway regulators Bax, Bcl-2, and Cytochrome-c genes in cortex and hippocampus across different experimental epilepsy models (Pentylenetetrazole-PTZ, Kindling, and Absence Epilepsy), in a tissue-and seizure-type-specific manner.Materials and Methods: In the study, male Wistar albino rats were used to establish PTZ (50 mg/kg) and Kindling (repeated PTZ injections at 35 mg/kg) models, whereas male WAG/Rij rats were employed as a genetic absence epilepsy model (n=8/group). Seizure severity in the animals was assessed according to the modified Racine scale. The levels of expression for the Bax, Bcl-2, and Cytochrome-c genes in cortical and hippocampal tissues were measured by Real-Time Polymerase Chain Reaction.Results: Compared to the control group, cortical Bax expression increased 1.64-fold in the absence epilepsy group, whereas hippocampal Bax expression increased 2.97-fold only in the PTZ group. The expression of the Bcl-2 gene was unchanged in the cortex but was significantly reduced by 0.49-fold and 0.30-fold in the hippocampus for PTZ and Kindling models, respectively. Cytochrome-c expression decreased significantly only in the cortex across all epilepsy models.Conclusion: The findings confirm that apoptotic gene expression exhibits region-specific variations depending on the epilepsy model and brain tissue. The disruption of the pro-apoptotic/anti-apoptotic balance (increase in Bax, decrease in Bcl-2) in the hippocampus in both acute and chronic seizure models suggests the involvement of the mitochondrial-mediated neuronal death pathway in these regions.