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首页> 外文期刊>The European Journal of Neuroscience >Gene expression pathways induced by axotomy and decentralization of rat superior cervical ganglion neurons.
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Gene expression pathways induced by axotomy and decentralization of rat superior cervical ganglion neurons.

机译：大鼠上颈神经节神经元轴突切开和分散诱导的基因表达途径。

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摘要

To identify genes potentially involved in remodelling synaptic connections, we induced the temporary detachment of pre- and post-synaptic elements by axotomy or denervation of rat superior cervical ganglion neurons. cDNA microarray analysis followed by stringent selection criteria allowed the identification of a panel of genes whose expression was modulated by axotomy at various time points after injury. Among these genes, 11 were validated by real-time reverse transcriptase-polymerase chain reaction on independently prepared samples after superior cervical ganglion neuron axotomy (1, 3 and 6 days) and compared with the effect of decentralization (8 h, 1 and 3 days). These genes code for extracellular matrix/space [apolipoprotein D (apoD), decorin, collagen alpha1 type I, collagen alpha1 type III] and intermediate filament (vimentin) proteins, for modulators of neurite outgrowth (thrombin receptor, plasminogen activator inhibitor-1, bone morphogenetic protein 4, annexin II and S-100-related protein, clone 42C) and for a nerve cell transcription factor (brain finger protein). Eight of these 11 genes showed significant and persistent modulations after both types of injury. Finally, protein levels of apoD were shown to increase in superior cervical ganglion after axotomy. Our results identify hitherto unrecorded genes responsive to axotomy and decentralization of superior cervical ganglion neurons, and probably involved in synapse formation, remodelling and elimination.
机译：为了鉴定潜在参与重塑突触连接的基因，我们通过大鼠上颈神经节神经元的轴突切开术或神经支配术诱导了突触前和突触后元素的暂时脱离。 cDNA微阵列分析和严格的选择标准允许鉴定一组基因，这些基因的表达在受伤后的各个时间点均由轴切术调节。在这些基因中，通过对上颈神经节神经元轴突切开术（1、3和6天）对独立制备的样品进行实时逆转录酶-聚合酶链反应验证了11个基因，并与分散作用（8小时，1和3天）进行了比较）。这些基因编码细胞外基质/空间[载脂蛋白D（apoD），核心蛋白聚糖，I型胶原alpha1，III型胶原alpha1]和中间丝（波形蛋白）蛋白，用于神经突增生的调节剂（凝血酶受体，纤溶酶原激活物抑制剂1，骨形态发生蛋白4，膜联蛋白II和S-100相关蛋白，克隆42C）和神经细胞转录因子（脑指蛋白）。在这两种类型的损伤后，这11个基因中有8个显示出明显且持续的调节。最后，轴突切开后，在上颈神经节中apoD的蛋白质水平升高。我们的结果确定了迄今为止尚未记录的对上颈神经节神经元的轴突切开和分散反应的基因，并且可能参与了突触的形成，重塑和消除。

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