Expression of the proto-oncogene bcl-2 is increased in the rat brain following kainate-induced seizures

Issue title: Oxidative Stress, Apoptosis and Brain Damage

Article type: Research Article

Authors: Graham, Steven H.^; | Chen, Jun | Stetler, R. Anne | Zhu, R. Li | Jin, Kun Lin | Simon, Roger P.

Affiliations: Department of Neurology, University of Pittsburgh, 325 Scaife Hall, Pittsburgh, PA 15261, USA | Neurology Service (127), Pittsburgh (University Drive), Veterans Affairs Medical Center, Pittsburgh, PA, USA

Note: [] Tel: +1-412-6489212; Fax; + 1-412-6481239; E-mail: sgra@pitt.edu

Abstract: The proto-oncogene bcl-2 is an important suppressor of apoptotic cell death in development and of both apoptotic and necrotic cell death in mature neurons. We studied expression of bcl-2 and the related gene, bax, which may promote cell death, after seizures induced by systemic kainate injection in rats. Expression of bcl-2 mRNA was studied by in situ hybridization. Bax and bcl-2 protein expression was studied by immunocytochemistry. Histologic analysis of cresyl violet-stained paraffin sections was performed at 72 h. bcl-2 protein was expressed in CA1 neurons, a region that is injured, yet survives after seizures. Bcl-2 mRNA was expressed in CA3, a region where there is extensive neuronal death at 72 h, but the bcl-2 protein was not translated. However, bax protein expression in CA3 was increased at 24 h. These results support a possible role for bcl-2 in promoting survival of CA3 after seizures.

Keywords: Apoptosis, Epilepsy, bcl-2, bcl-x, Hippocampus

DOI: 10.3233/RNN-1996-9407

Journal: Restorative Neurology and Neuroscience, vol. 9, no. 4, pp. 243-250, 1996