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首页> 外文期刊>CNS neuroscience & therapeutics. >Increased Activation of Synapsin 1 and Mitogen‐Activated Protein Kinases/Extracellular Signal‐Regulated Kinase in the Amygdala of Maternal Separation Rats
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Increased Activation of Synapsin 1 and Mitogen‐Activated Protein Kinases/Extracellular Signal‐Regulated Kinase in the Amygdala of Maternal Separation Rats

机译：母体分离大鼠杏仁核中突触蛋白1和丝裂原激活的蛋白激酶/细胞外信号调节激酶的激活增加

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Summary Background Early life stress ( ELS ) causes alterations in emotionality and anxiety levels as a significant risk factor for psychiatric problems, and these alterations have been associated with amygdala activity. Aims To elucidate the molecular mechanism on the development of psychiatric problems following ELS , we identified the alteration of molecules in the amygdala using maternal separation ( MS ; pnd 14–21) rats through gene expression and DNA methylation microarray analysis, and studied the involvement of candidate genes using a Western blot and immunohistochemistry analysis. Results Through a microarray analysis, in the amygdala of MS rats, we found a downregulation of mRNA expression of synapsin 1 (Syn1) gene with hypermethylation of its transcription start site (TSS), and the alterations of mRNA expressions of Syn1 activation‐related kinase genes including mitogen‐activated protein kinases (Mapks) with change of their TSS methylation. In addition, MS increased not only Syn1 phosphorylation at the phosphorylation sites by Mapk/extracellular signal‐regulated kinase (Erk), but also Mapk/Erk phosphorylation in the amygdala. Furthermore, double immunofluorescence staining showed that MS could elevate phospho‐Mapk/Erk immunoreactivity (IR) in Syn1‐expression puncta. Conclusion These findings indicated that the activation of Mapk/Erk and Syn1 may be a key mechanism modulating synaptic neurotransmition in the amygdala of MS rats.
机译：背景技术早期生活压力（ELS）引起情绪和焦虑水平的改变，这是精神疾病的重要危险因素，这些改变与杏仁核活动有关。目的为了阐明ELS引起的精神疾病发展的分子机制，我们通过基因表达和DNA甲基化微阵列分析，使用母本分离（MS; pnd 14-21）大鼠鉴定了杏仁核中分子的改变，并研究了使用蛋白质印迹和免疫组化分析的候选基因。结果通过微阵列分析，在MS大鼠的杏仁核中，我们发现突触素1（Syn1）基因的mRNA表达下调，其转录起始位点（TSS）甲基化，并且Syn1激活相关激酶的mRNA表达发生变化TSS甲基化变化的基因，包括促分裂原激活的蛋白激酶（Mapks）。此外，MS不仅通过Mapk /细胞外信号调节激酶（Erk）增强了磷酸化位点上的Syn1磷酸化，而且还增强了杏仁核中的Mapk / Erk磷酸化。此外，双重免疫荧光染色显示MS可以提高Syn1表达点的磷酸化Mapk / Erk免疫反应性（IR）。结论这些发现表明，MAPK / Erk和Syn1的激活可能是调节MS大鼠杏仁核突触神经传递的关键机制。

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