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.
Restor Neurol Neurosci. 1996 Jan 1;9(4):243-50. doi: 10.3233/RNN-1996-9407.
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.
原癌基因 bcl-2 是发育过程中细胞凋亡和成熟神经元中细胞凋亡和坏死的重要抑制剂。我们研究了在大鼠全身注射海人酸诱导的癫痫发作后,bcl-2 和可能促进细胞死亡的相关基因 bax 的表达。通过原位杂交研究 bcl-2 mRNA 的表达。通过免疫细胞化学研究 Bax 和 bcl-2 蛋白的表达。在 72 小时时,对经亚甲蓝染色的石蜡切片进行组织学分析。bcl-2 蛋白在 CA1 神经元中表达,CA1 是癫痫发作后受损但存活的区域。bcl-2 mRNA 在 CA3 中表达,CA3 在 72 小时时有广泛的神经元死亡,但 bcl-2 蛋白未被翻译。然而,CA3 中的 bax 蛋白表达在 24 小时时增加。这些结果支持 bcl-2 在促进癫痫发作后 CA3 存活中的可能作用。