The role of bcl-2 family of genes during kindling

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Updated: Aug 19, 2026

Examining BCL-2 Family Function with Large Unilamellar Vesicles
08:35

Examining BCL-2 Family Function with Large Unilamellar Vesicles

Published on: October 5, 2012

Kamil Can Akcali1, Melike Sahiner, Turker Sahiner

  • 1Department of Molecular Biology and Genetics, Bilkent University, Ankara, Turkey. akcali@fen.bilkent.edu.tr

Epilepsia
|February 1, 2005
PubMed
Abstract

Insights

This study reveals that Bax and Bcl-xL gene expression changes during epilepsy development in rats. These alterations in apoptotic regulators may contribute to neuronal changes without immediate DNA fragmentation.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Epilepsy Research

Background:

  • Apoptotic neuronal death is implicated in temporal lobe epilepsy.
  • The role of apoptotic regulators during epileptogenesis remains unclear.

Purpose of the Study:

  • Investigate the expression patterns of bcl-2 family genes during the development of the kindling model of epilepsy in rats.
  • Clarify the role of apoptotic regulators in epileptogenesis.

Main Methods:

  • Examined mRNA and protein levels of bax, bcl-2, bcl-xL, mtd, and bcl-w in rat brain tissues.
  • Utilized the kindling model to induce epilepsy in adult rats.
  • Assessed DNA fragmentation using the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay.

Main Results:

  • Epileptic discharges began around day 10 of the kindling model.
  • Bax (apoptosis inducer) expression increased, while Bcl-xL (apoptosis inhibitor) expression decreased during epilepsy formation.
  • No DNA fragmentation was detected via TUNEL staining.

Conclusions:

  • Differential expression of Bax and Bcl-xL occurs in the CA1 region during hippocampal kindling.
  • Altered Bax and Bcl-xL expression suggests a potential mechanism for inducing DNA fragmentation in neurons during epileptogenesis, even without observable fragmentation.

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