Differential expression of synaptic vesicle proteins after repeated electroconvulsive seizures in rat frontal cortex and hippocampus

Differential expression of synaptic vesicle proteins after repeated electroconvulsive seizures in rat frontal cortex and hippocampus
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DOI:
10.1002/syn.20538
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发表时间:
2008-09-01
期刊:
影响因子:
2.3
通讯作者:
Wegener, Gregers
Wegener, Gregers
中科院分区:
医学4区
文献类型:
--
作者:
Elfving, Betina;Bonefeld, Birgit Egeskov;Wegener, Gregers

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电休克治疗(ECT)仍然是重度或耐药抑郁症患者的治疗选择,但其疗效背后的机制和对神经传递的影响基本上是未知的。由于突触囊泡蛋白(SVP)是囊泡融合和神经递质释放所必需的,我们研究了单次和重复电惊厥发作(ECS),ECT的动物模型,对大鼠额叶皮层和海马中14个SVP表达的影响,使用定量实时聚合酶链反应(实时qPCR)。只有在额叶皮层,突触蛋白11的mRNA水平显着上调后,重复ECS。与此相反,ECS后,14个SVP中的6个的mRNA水平在海马中显著调节。我们发现,SNAP 29上调和synaptotagmin III下调后,一个单一的ECS在海马。此外,SNAP 29,突触蛋白I,突触蛋白III,VAMP 2和VAMP 5显着上调,而突触结合蛋白III显着下调后,在海马重复ECS。我们认为这些基因在ECS的长期治疗效果中非常重要,因此可以假设SVP参与了抑郁症的病理生理学。
Electroconvulsive therapy (ECT) remains the treatment of choice for patients with severe or drug-resistant depressive disorders, yet the mechanism behind its efficacy and the effect on neurotransmission is essentially unknown. As synaptic vesicle proteins (SVPs) are required for vesicle fusion and neurotransmitter release, we have examined the effect of single and repeated electroconvulsive seizures (ECS), an animal model of ECT, on the expression of 14 SVPs in the rat frontal cortex and the hippocampus using quantitative real-time polymerase chain reaction (real-time qPCR). Only in the frontal cortex, the mRNA level of synapsin 11 was significantly upregulated after repeated ECS. In contrast, the mRNA levels of 6 of the 14 SVPs were significantly regulated in the hippocampus after ECS. We found that SNAP29 was upregulated and synaptotagmin III was downregulated after one single ECS in the hippocampus. Furthermore, SNAP29, synapsin I, synapsin III, VAMP2, and VAMP5 were significantly upregulated, whereas synaptotagmin III was significantly downregulated after repeated ECS in the hippocampus. We suggest that these genes are highly important in the long-term therapeutic effect of ECS, and thus it can be hypothesized that the SVPs are involved in the pathophysiology of depression.