Sun H B, Yokota H, Chi X X, Xu Z C
Department of Anatomy and Cell Biology, Indiana University School of Medicine, 635 Barnhill Drive, Indianapolis, IN 46202, USA.
Brain Res Mol Brain Res. 2000 Dec 8;84(1-2):146-9. doi: 10.1016/s0169-328x(00)00237-0.
A short period of cerebral ischemia will trigger a cascade of events leading to neuronal death. In an effort to elucidate molecular mechanisms underlying differential vulnerability of CA1 and CA3 hippocampal neurons to neurodegeneration, we performed a transcriptional analysis of rat hippocampal neurons following transient global ischemia. In response to 15-min ischemia, the mRNA level of neurexins II alpha and III alpha was elevated in CA1 neurons and CA3 neurons, respectively. Interestingly, the up-regulated neurexin III alpha mRNA in postischemic CA3 consisted of the insert corresponding to the fourth splicing site, while the transcripts in postischemic CA1 neurons and control CA3 neurons lacked the insert. The observed tissue specific expression and the splicing pattern suggest functional importance of neurexins in postischemic degeneration of hippocampal neurons.
短暂的脑缺血会引发一系列导致神经元死亡的事件。为了阐明海马体CA1和CA3神经元对神经退行性变的不同易损性背后的分子机制,我们对短暂性全脑缺血后的大鼠海马神经元进行了转录分析。在15分钟的缺血反应中,神经连接蛋白IIα和IIIα的mRNA水平分别在CA1神经元和CA3神经元中升高。有趣的是,缺血后CA3中上调的神经连接蛋白IIIα mRNA由对应于第四个剪接位点的插入片段组成,而缺血后CA1神经元和对照CA3神经元中的转录本则缺乏该插入片段。观察到的组织特异性表达和剪接模式表明神经连接蛋白在海马神经元缺血后变性中具有重要功能。